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  1 / 2978 MEDLINE  
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[PMID]:29022673
[Au] Autor:Angeletti A; Marasà M; Cravedi P
[Ad] Dirección:University of Bologna, Bologna, Italy
[Ti] Título:CD55 Deficiency and Protein-Losing Enteropathy.
[So] Fuente:N Engl J Med;377(15):1499, 2017 10 12.
[Is] ISSN:1533-4406
[Cp] País de publicación:United States
[La] Idioma:eng
[Mh] Términos MeSH primario: Procedimiento de Fontan
Enteropatías Perdedoras de Proteínas
[Mh] Términos MeSH secundario: Seres Humanos
[Pt] Tipo de publicación:LETTER; COMMENT
[Em] Mes de ingreso:1710
[Cu] Fecha actualización por clase:171018
[Lr] Fecha última revisión:171018
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:171013
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1710011


  2 / 2978 MEDLINE  
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[PMID]:29020582
[Au] Autor:Kurolap A; Eshach-Adiv O; Baris HN
[Ad] Dirección:Technion-Israel Institute of Technology, Haifa, Israel.
[Ti] Título:CD55 Deficiency and Protein-Losing Enteropathy.
[So] Fuente:N Engl J Med;377(15):1500, 2017 10 12.
[Is] ISSN:1533-4406
[Cp] País de publicación:United States
[La] Idioma:eng
[Mh] Términos MeSH primario: Procedimiento de Fontan
Enteropatías Perdedoras de Proteínas
[Mh] Términos MeSH secundario: Seres Humanos
[Pt] Tipo de publicación:LETTER; COMMENT
[Em] Mes de ingreso:1710
[Cu] Fecha actualización por clase:171018
[Lr] Fecha última revisión:171018
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:171012
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1710011


  3 / 2978 MEDLINE  
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[PMID]:29020581
[Au] Autor:Ozen A; Comrie WA; Lenardo MJ
[Ad] Dirección:Marmara University, Istanbul, Turkey
[Ti] Título:CD55 Deficiency and Protein-Losing Enteropathy.
[So] Fuente:N Engl J Med;377(15):1499-1500, 2017 10 12.
[Is] ISSN:1533-4406
[Cp] País de publicación:United States
[La] Idioma:eng
[Mh] Términos MeSH primario: Procedimiento de Fontan
Enteropatías Perdedoras de Proteínas
[Mh] Términos MeSH secundario: Seres Humanos
[Pt] Tipo de publicación:LETTER; COMMENT
[Em] Mes de ingreso:1710
[Cu] Fecha actualización por clase:171018
[Lr] Fecha última revisión:171018
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:171012
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1710011


  4 / 2978 MEDLINE  
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[PMID]:28657861
[Au] Autor:Kurolap A; Eshach-Adiv O; Hershkovitz T; Paperna T; Mory A; Oz-Levi D; Zohar Y; Mandel H; Chezar J; Azoulay D; Peleg S; Half EE; Yahalom V; Finkel L; Weissbrod O; Geiger D; Tabib A; Shaoul R; Magen D; Bonstein L; Mevorach D; Baris HN
[Ad] Dirección:Technion-Israel Institute of Technology, Haifa, Israel.
[Ti] Título:Loss of CD55 in Eculizumab-Responsive Protein-Losing Enteropathy.
[So] Fuente:N Engl J Med;377(1):87-89, 2017 07 06.
[Is] ISSN:1533-4406
[Cp] País de publicación:United States
[La] Idioma:eng
[Mh] Términos MeSH primario: Anticuerpos Monoclonales Humanizados/uso terapéutico
Antígenos CD55/genética
Mutación del Sistema de Lectura
Enteropatías Perdedoras de Proteínas/tratamiento farmacológico
Enteropatías Perdedoras de Proteínas/genética
[Mh] Términos MeSH secundario: Niño
Preescolar
Ensayos de Uso Compasivo
Activación de Complemento
Complejo de Ataque a Membrana del Sistema Complemento/metabolismo
Diarrea/etiología
Femenino
Seres Humanos
Masculino
Mediana Edad
Linaje
Análisis de Secuencia de ADN
Albúmina Sérica/metabolismo
Adulto Joven
[Pt] Tipo de publicación:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nombre de substancia:
0 (Antibodies, Monoclonal, Humanized); 0 (CD55 Antigens); 0 (Complement Membrane Attack Complex); 0 (Serum Albumin); A3ULP0F556 (eculizumab)
[Em] Mes de ingreso:1707
[Cu] Fecha actualización por clase:171116
[Lr] Fecha última revisión:171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:170629
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1707173


  5 / 2978 MEDLINE  
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[PMID]:28657829
[Au] Autor:Ozen A; Comrie WA; Ardy RC; Domínguez Conde C; Dalgic B; Beser ÖF; Morawski AR; Karakoc-Aydiner E; Tutar E; Baris S; Ozcay F; Serwas NK; Zhang Y; Matthews HF; Pittaluga S; Folio LR; Unlusoy Aksu A; McElwee JJ; Krolo A; Kiykim A; Baris Z; Gulsan M; Ogulur I; Snapper SB; Houwen RHJ; Leavis HL; Ertem D; Kain R; Sari S; Erkan T; Su HC; Boztug K; Lenardo MJ
[Ad] Dirección:From the Section of Molecular Development of the Immune System, Laboratory of Immunology (A.O., W.A.C., A.R.M., H.F.M., M.J.L.), the Clinical Genomics Program (A.O., W.A.C., A.R.M., Y.Z., H.F.M., H.C.S., M.J.L.), and the Human Immunological Diseases Section, Laboratory of Host Defenses (Y.Z., H.C.S.
[Ti] Título:CD55 Deficiency, Early-Onset Protein-Losing Enteropathy, and Thrombosis.
[So] Fuente:N Engl J Med;377(1):52-61, 2017 07 06.
[Is] ISSN:1533-4406
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:BACKGROUND: Studies of monogenic gastrointestinal diseases have revealed molecular pathways critical to gut homeostasis and enabled the development of targeted therapies. METHODS: We studied 11 patients with abdominal pain and diarrhea caused by early-onset protein-losing enteropathy with primary intestinal lymphangiectasia, edema due to hypoproteinemia, malabsorption, and less frequently, bowel inflammation, recurrent infections, and angiopathic thromboembolic disease; the disorder followed an autosomal recessive pattern of inheritance. Whole-exome sequencing was performed to identify gene variants. We evaluated the function of CD55 in patients' cells, which we confirmed by means of exogenous induction of expression of CD55. RESULTS: We identified homozygous loss-of-function mutations in the gene encoding CD55 (decay-accelerating factor), which lead to loss of protein expression. Patients' T lymphocytes showed increased complement activation causing surface deposition of complement and the generation of soluble C5a. Costimulatory function and cytokine modulation by CD55 were defective. Genetic reconstitution of CD55 or treatment with a complement-inhibitory therapeutic antibody reversed abnormal complement activation. CONCLUSIONS: CD55 deficiency with hyperactivation of complement, angiopathic thrombosis, and protein-losing enteropathy (the CHAPLE syndrome) is caused by abnormal complement activation due to biallelic loss-of-function mutations in CD55. (Funded by the National Institute of Allergy and Infectious Diseases and others.).
[Mh] Términos MeSH primario: Antígenos CD55/genética
Activación de Complemento/genética
Proteínas del Sistema Complemento/metabolismo
Mutación
Enteropatías Perdedoras de Proteínas/genética
Trombosis/genética
[Mh] Términos MeSH secundario: Antígenos CD55/sangre
Niño
Preescolar
Activación de Complemento/efectos de los fármacos
Inactivadores del Complemento/farmacología
Femenino
Homocigoto
Seres Humanos
Inmunoglobulina A/sangre
Lactante
Intestino Delgado/patología
Masculino
Linaje
Enteropatías Perdedoras de Proteínas/complicaciones
Estadísticas no Paramétricas
Síndrome
Linfocitos T/metabolismo
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
0 (CD55 Antigens); 0 (Complement Inactivating Agents); 0 (Immunoglobulin A); 9007-36-7 (Complement System Proteins)
[Em] Mes de ingreso:1707
[Cu] Fecha actualización por clase:171116
[Lr] Fecha última revisión:171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:170629
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMoa1615887


  6 / 2978 MEDLINE  
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[PMID]:28625042
[Au] Autor:Dwipoerwantoro PG; Lukito W; Aulia D; Arnaud J; Roussel AM
[Ad] Dirección:Gastrohepatology Division, Department of Child Health, Faculty of Medicine - Universitas Indonesia, Dr. Cipto Mangunkusumo General Hospital, Jakarta, Indonesia. Email: pramitagd@yahoo.com.
[Ti] Título:Selenium status and fungi in the protein-losing enteropathy of persistent diarrhea.
[So] Fuente:Asia Pac J Clin Nutr;26(Suppl 1):S79-S84, 2017 Jun.
[Is] ISSN:0964-7058
[Cp] País de publicación:Australia
[La] Idioma:eng
[Ab] Resumen:BACKGROUND AND OBJECTIVES: A vicious cycle of infection, malabsorption, and malnutrition has been implicated in the perpetuation of diarrheal disease. This study examined whether persistent diarrhea is associated with changes in selenium status and stool alpha-1 antitrypsin (AAT) concentration. METHODS AND STUDY DESIGN: This cross-sectional study included 30 children aged 1-12 years with persistent diarrhea who were hospitalized in Cipto Mangunkusumo Hospital and Fatmawati Hospital, Jakarta, and 30 apparently healthy children who were matched by age and sex and lived in a rural area of Jakarta. Clinical examinations, blood routine tests, erythrocyte glutathione peroxidase (GPX) activity and plasma selenium levels as well as AAT in fresh stool samples were performed in all the subjects. RESULTS: Of 30 children with persistent diarrhea, 17 had moderate malnutrition and 13 had severe malnutrition. The mean plasma selenium was significantly lower in children with persistent diarrhea than in children without diarrhea (86.0 µg/L [95% CI: 76.1-95.9] vs 110 µg/L [95% CI: 104-116, p<0.0001). The mean stool AAT concentration was significantly higher in children with persistent diarrhea than in those without diarrhea (115 mg/dL [95% CI: 38.5-191] vs 16 mg/dL [95% CI: 4.0-13.5, p<0.0001]). Selenium correlated with AAT (p=0.05). Fecal fungi were persistently present. CONCLUSIONS: Although selenium status in both groups was optimal for the obtained plasma GPX activity, children with persistent diarrhea exhibited lower plasma selenium levels. This study suggests that the decrease in the plasma selenium level may be the consequence of protein loss and that fungi may be involved.
[Mh] Términos MeSH primario: Diarrea/etiología
Micosis/complicaciones
Enteropatías Perdedoras de Proteínas/patología
Selenio/sangre
[Mh] Términos MeSH secundario: Biomarcadores
Niño
Preescolar
Estudios Transversales
Heces/química
Femenino
Seres Humanos
Lactante
Masculino
Enteropatías Perdedoras de Proteínas/sangre
Enteropatías Perdedoras de Proteínas/etiología
Selenio/deficiencia
alfa 1-Antitripsina/química
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Nm] Nombre de substancia:
0 (Biomarkers); 0 (alpha 1-Antitrypsin); H6241UJ22B (Selenium)
[Em] Mes de ingreso:1708
[Cu] Fecha actualización por clase:170831
[Lr] Fecha última revisión:170831
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170620
[St] Status:MEDLINE
[do] DOI:10.6133/apjcn.062017.s13


  7 / 2978 MEDLINE  
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[PMID]:28619193
[Au] Autor:Itkin M; Piccoli DA; Nadolski G; Rychik J; DeWitt A; Pinto E; Rome J; Dori Y
[Ad] Dirección:Center for Lymphatic Imaging and Interventions, Children's Hospital of Philadelphia/Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address: itkinmax@gmail.com.
[Ti] Título:Protein-Losing Enteropathy in Patients With Congenital Heart Disease.
[So] Fuente:J Am Coll Cardiol;69(24):2929-2937, 2017 Jun 20.
[Is] ISSN:1558-3597
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:BACKGROUND: Protein-losing enteropathy (PLE), characterized by loss of proteins in the intestine, is a devastating complication in patients with congenital heart disease. The cause of PLE is unknown, but lymphatic involvement has been suspected. OBJECTIVES: The authors evaluated the use of lymphangiographic imaging and liver lymphatic embolization as a treatment for PLE. METHODS: This was a single-center, retrospective review of imaging and interventions used in 8 consecutive patients with liver lymphatic embolization and congenital heart disease with elevated central venous pressure complicated by PLE. RESULTS: Liver lymphangiography was performed in 8 patients (5 males, 3 females; median age, 21 years), 7 of whom demonstrated leakage of liver lymph into the duodenum through abnormal hepatoduodenal lymphatic communications. This was confirmed by duodenoscopy with simultaneous injection of isosulfan blue dye into the liver lymphatics in 6 of 7 patients. Liver lymphatic embolization with ethiodized oil in 2 patients resulted in a temporary increase in albumin blood level and symptom improvement in 1 patient, but was complicated by duodenal bleeding in both patients. Of the remaining 6 patients, liver lymphatic embolization with n-butyl cyanoacrylate glue resulted in sustained improvement of the serum albumin level and symptoms in 3 patients, temporary improvement in 2 patients, and no change in 1 patient with median follow-up of 135 days (range, 84 to 1,005 days). CONCLUSIONS: The authors demonstrated liver lymph leakage as a cause of PLE in patients with congenital heart disease and elevated central venous pressure. Lymphatic embolization led to improved albumin levels and relief of symptoms. Further experience with the technique is needed to determine long-term outcome of this procedure.
[Mh] Términos MeSH primario: Embolización Terapéutica/métodos
Cardiopatías Congénitas/complicaciones
Enteropatías Perdedoras de Proteínas/etiología
[Mh] Términos MeSH secundario: Adolescente
Adulto
Niño
Preescolar
Femenino
Estudios de Seguimiento
Seres Humanos
Linfografía
Masculino
Mediana Edad
Enteropatías Perdedoras de Proteínas/diagnóstico
Enteropatías Perdedoras de Proteínas/cirugía
Estudios Retrospectivos
Resultado del Tratamiento
Adulto Joven
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1708
[Cu] Fecha actualización por clase:170816
[Lr] Fecha última revisión:170816
[Sb] Subgrupo de revista:AIM; IM
[Da] Fecha de ingreso para procesamiento:170617
[St] Status:MEDLINE


  8 / 2978 MEDLINE  
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[PMID]:28541008
[Au] Autor:Ahn WK; Park S; Kim HD
[Ad] Dirección:Division of Pediatric Neurology, Department of Pediatrics, Severance Children's Hospital, Yonsei University College of Medicine, Seoul, Korea.
[Ti] Título:Protein-Losing Enteropathy as a Complication of the Ketogenic Diet.
[So] Fuente:Yonsei Med J;58(4):891-893, 2017 Jul.
[Is] ISSN:1976-2437
[Cp] País de publicación:Korea (South)
[La] Idioma:eng
[Ab] Resumen:The ketogenic diet is an effective treatment for the patients with intractable epilepsy, however, the diet therapy can sometimes be discontinued by complications. Protein-losing enteropathy is a rarely reported serious complication of the ketogenic diet. We present a 16-month-old Down syndrome baby with protein-losing enteropathy during the ketogenic diet as a treatment for West syndrome. He suffered from diarrhea, general edema and hypoalbuminemia which were not controlled by conservative care for over 1 month. Esophagogastroduodenoscopy and stool alpha-1 antitrypsin indicated protein-losing enteropathy. Related symptoms were relieved after cessation of the ketogenic diet. Unexplained hypoalbuminemia combined with edema and diarrhea during ketogenic suggests the possibility of protein-losing enteropathy, and proper evaluation is recommended in order to expeditiously detect it and to act accordingly.
[Mh] Términos MeSH primario: Dieta Cetogénica/efectos adversos
Enteropatías Perdedoras de Proteínas/complicaciones
[Mh] Términos MeSH secundario: Duodeno/patología
Seres Humanos
Lactante
Masculino
Membrana Mucosa/patología
Apoyo Nutricional
[Pt] Tipo de publicación:CASE REPORTS
[Em] Mes de ingreso:1710
[Cu] Fecha actualización por clase:171116
[Lr] Fecha última revisión:171116
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170526
[St] Status:MEDLINE
[do] DOI:10.3349/ymj.2017.58.4.891


  9 / 2978 MEDLINE  
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[PMID]:28534240
[Au] Autor:Unseld B; Stiller B; Borth-Bruhns T; du Bois F; Kroll J; Grohmann J; Fleck T
[Ad] Dirección:Department of Congenital Heart Disease and Pediatric Cardiology, University Heart Centre Freiburg, Mathildenstrasse 1, 79106, Freiburg, Germany.
[Ti] Título:An Early Glenn Operation May be Associated with the Later Occurrence of Protein-Losing Enteropathy in Fontan Patients : Association of Early Glenn and Failing Fontan.
[So] Fuente:Pediatr Cardiol;38(6):1155-1161, 2017 Aug.
[Is] ISSN:1432-1971
[Cp] País de publicación:United States
[La] Idioma:eng
[Ab] Resumen:Protein-losing enteropathy (PLE) and plastic bronchitis (PB) are major causes of long-term mortality after Fontan operation. The objective of this study was to determine early clinical risk factors before the onset of PLE and PB. In a cohort study, 106 Fontan patients between 2005 and 2013 were examined. A median of 5.3 (1.5-8.5) years later, follow-up questionnaires were used to group the patients in a PLE or PB group (n = 14) and a non-PLE/PB group (n = 92). Prevalence of PLE was 9.4% (n = 10) and of PB 3.8% (n = 4). At follow-up, five patients (4.7%) died of PLE or PB. Median age at death was 6.2 years (IQR 10.5, 95% CI 5.3-23.4). We observed no significant group differences in gender distribution (p = 0.73), ventricular morphology (p = 0.87), surgical technique (p = 0.64), conduit fenestration (p = 0.34), age at Fontan operation (p = 0.54), and need for diuretics (p = 0.56). Hypoplastic left heart syndrome was more frequent in the PLE/PB group 50 vs. 22.8% (p = 0.03) OR 3.4 (95% CI 1.1-10.8). The modified Glenn procedure was performed at a median age of 4 months (IQR 4.0) in the PLE/PB group versus 8 months (IQR 8.0) in the non-PLE/PB group (p = 0.01). The early Glenn procedure and hypoplastic left heart syndrome may be associated with the development of PLE and PB.
[Mh] Términos MeSH primario: Procedimiento de Fontan/efectos adversos
Cardiopatías Congénitas/cirugía
Enteropatías Perdedoras de Proteínas/etiología
[Mh] Términos MeSH secundario: Bronquitis/etiología
Niño
Preescolar
Femenino
Procedimiento de Fontan/rehabilitación
Cardiopatías Congénitas/rehabilitación
Seres Humanos
Síndrome del Corazón Izquierdo Hipoplásico/rehabilitación
Síndrome del Corazón Izquierdo Hipoplásico/cirugía
Lactante
Masculino
Estudios Retrospectivos
Factores de Riesgo
Encuestas y Cuestionarios
Factores de Tiempo
Procedimientos Quirúrgicos Vasculares/efectos adversos
Procedimientos Quirúrgicos Vasculares/rehabilitación
[Pt] Tipo de publicación:JOURNAL ARTICLE
[Em] Mes de ingreso:1709
[Cu] Fecha actualización por clase:170914
[Lr] Fecha última revisión:170914
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170524
[St] Status:MEDLINE
[do] DOI:10.1007/s00246-017-1632-7


  10 / 2978 MEDLINE  
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Chebli, Júlio Maria Fonseca
Texto completo SciELO Brasil
[PMID]:28489125
[Au] Autor:Chebli JMF; Chebli LA; Ribeiro TCDR; Gaburri PD
[Ad] Dirección:Gastroenterology Professor at School of Medicine of Universidade Federal de Juiz de Fora, Juiz de Fora, MG, Brazil.
[Ti] Título:Severe hypoproteinemia as a harbinger of Ménétrier's disease in autoimmune pancreatitis.
[So] Fuente:Rev Assoc Med Bras (1992);63(3):215-218, 2017 Mar.
[Is] ISSN:1806-9282
[Cp] País de publicación:Brazil
[La] Idioma:eng
[Ab] Resumen:Ménétrier's disease is an extremely rare disease of unknown etiology causing gastric mucosal hypertrophy and protein-losing gastropathy. Rare cases of this condition have been reported in patients with autoimmune diseases. However, to the best of our knowledge, Ménétrier's disease associated with autoimmune pancreatitis (AIP) has never been reported. We described a case of severe hypoproteinemia as a harbinger of Ménétrier's disease associated with AIP. The patient was successfully treated with octreotide and high-protein diet, which led to symptomatic remission and significant improvement in serum levels of albumin and recovery of the nutritional status. Thus, in AIP patients presenting with severe and persistent hypoproteinemia without apparent cause, clinicians need to consider Ménétrier's disease in the differential diagnosis. In this setting, endoscopic evaluation with histological examination of gastric biopsy material, including a full-thickness mucosal biopsy of involved mucosa, may be helpful in promptly establishing the diagnosis and allowing appropriate and timely therapy.
[Mh] Términos MeSH primario: Enfermedades Autoinmunes/complicaciones
Gastritis Hipertrófica/complicaciones
Hipoproteinemia/etiología
Pancreatitis/complicaciones
[Mh] Términos MeSH secundario: Enfermedades Autoinmunes/sangre
Enfermedades Autoinmunes/patología
Biopsia
Endoscopía Gastrointestinal
Mucosa Gástrica/patología
Gastritis Hipertrófica/sangre
Gastritis Hipertrófica/patología
Seres Humanos
Hipoproteinemia/patología
Masculino
Mediana Edad
Pancreatitis/sangre
Pancreatitis/patología
Índice de Severidad de la Enfermedad
[Pt] Tipo de publicación:CASE REPORTS
[Em] Mes de ingreso:1708
[Cu] Fecha actualización por clase:170829
[Lr] Fecha última revisión:170829
[Sb] Subgrupo de revista:IM
[Da] Fecha de ingreso para procesamiento:170511
[St] Status:MEDLINE



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