Single nucleotide polymorphisms in AGTR1, TFAP2B, and TRAF1 are not associated with the incidence of patent ductus arteriosus in Japanese preterm infants
Background Persistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes, including angiotensin II receptor, type 1 (AGTR1), transcription factor AP‐2 beta (TFAP2B) and tumor necrosis factor receptor‐associated factor...
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Published in | Pediatrics international Vol. 58; no. 6; pp. 461 - 466 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Australia
Blackwell Publishing Ltd
01.06.2016
|
Subjects | |
Online Access | Get full text |
ISSN | 1328-8067 1442-200X 1442-200X |
DOI | 10.1111/ped.12861 |
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Abstract | Background
Persistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes, including angiotensin II receptor, type 1 (AGTR1), transcription factor AP‐2 beta (TFAP2B) and tumor necrosis factor receptor‐associated factor 1 (TRAF1), have been reported to be associated with PDA in preterm infants. The aim of this study was to evaluate the relationships between PDA in preterm infants and polymorphisms in AGTR1, TFAP2B and TRAF1 in the Japanese population.
Methods
The subjects consisted of 107 preterm infants with gestational age <32 weeks. Extremely low‐birthweight infants were treated with prophylactic indomethacin during the first 24 h after birth. Five SNP, namely, rs5186 in AGTR1, rs987237 and rs6930924 in TFAP2B, and rs1056567 and rs10985070 in TRAF1, were genotyped using TaqMan SNP genotyping assays.
Results
There were no significant differences in the distributions of the genotypes and allele frequencies of all studied SNP between the PDA group (n = 46) and the non‐PDA group (n = 61).
Conclusions
There were no significant associations between the studied SNP and the incidence of PDA in Japanese preterm infants. These SNP may not be clinically important predisposing factors for PDA in Japanese preterm infants. |
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AbstractList | Background Persistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes, including angiotensin II receptor, type 1 (AGTR1), transcription factor AP-2 beta (TFAP2B) and tumor necrosis factor receptor-associated factor 1 (TRAF1), have been reported to be associated with PDA in preterm infants. The aim of this study was to evaluate the relationships between PDA in preterm infants and polymorphisms in AGTR1, TFAP2B and TRAF1 in the Japanese population. Methods The subjects consisted of 107 preterm infants with gestational age <32weeks. Extremely low-birthweight infants were treated with prophylactic indomethacin during the first 24h after birth. Five SNP, namely, rs5186 in AGTR1, rs987237 and rs6930924 in TFAP2B, and rs1056567 and rs10985070 in TRAF1, were genotyped using TaqMan SNP genotyping assays. Results There were no significant differences in the distributions of the genotypes and allele frequencies of all studied SNP between the PDA group (n=46) and the non-PDA group (n=61). Conclusions There were no significant associations between the studied SNP and the incidence of PDA in Japanese preterm infants. These SNP may not be clinically important predisposing factors for PDA in Japanese preterm infants. BackgroundPersistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes, including angiotensin II receptor, type 1 (AGTR1), transcription factor AP‐2 beta (TFAP2B) and tumor necrosis factor receptor‐associated factor 1 (TRAF1), have been reported to be associated with PDA in preterm infants. The aim of this study was to evaluate the relationships between PDA in preterm infants and polymorphisms in AGTR1, TFAP2B and TRAF1 in the Japanese population.MethodsThe subjects consisted of 107 preterm infants with gestational age <32 weeks. Extremely low‐birthweight infants were treated with prophylactic indomethacin during the first 24 h after birth. Five SNP, namely, rs5186 in AGTR1, rs987237 and rs6930924 in TFAP2B, and rs1056567 and rs10985070 in TRAF1, were genotyped using TaqMan SNP genotyping assays.ResultsThere were no significant differences in the distributions of the genotypes and allele frequencies of all studied SNP between the PDA group (n = 46) and the non‐PDA group (n = 61).ConclusionsThere were no significant associations between the studied SNP and the incidence of PDA in Japanese preterm infants. These SNP may not be clinically important predisposing factors for PDA in Japanese preterm infants. Persistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes, including angiotensin II receptor, type 1 (AGTR1), transcription factor AP-2 beta (TFAP2B) and tumor necrosis factor receptor-associated factor 1 (TRAF1), have been reported to be associated with PDA in preterm infants. The aim of this study was to evaluate the relationships between PDA in preterm infants and polymorphisms in AGTR1, TFAP2B and TRAF1 in the Japanese population.BACKGROUNDPersistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes, including angiotensin II receptor, type 1 (AGTR1), transcription factor AP-2 beta (TFAP2B) and tumor necrosis factor receptor-associated factor 1 (TRAF1), have been reported to be associated with PDA in preterm infants. The aim of this study was to evaluate the relationships between PDA in preterm infants and polymorphisms in AGTR1, TFAP2B and TRAF1 in the Japanese population.The subjects consisted of 107 preterm infants with gestational age <32 weeks. Extremely low-birthweight infants were treated with prophylactic indomethacin during the first 24 h after birth. Five SNP, namely, rs5186 in AGTR1, rs987237 and rs6930924 in TFAP2B, and rs1056567 and rs10985070 in TRAF1, were genotyped using TaqMan SNP genotyping assays.METHODSThe subjects consisted of 107 preterm infants with gestational age <32 weeks. Extremely low-birthweight infants were treated with prophylactic indomethacin during the first 24 h after birth. Five SNP, namely, rs5186 in AGTR1, rs987237 and rs6930924 in TFAP2B, and rs1056567 and rs10985070 in TRAF1, were genotyped using TaqMan SNP genotyping assays.There were no significant differences in the distributions of the genotypes and allele frequencies of all studied SNP between the PDA group (n = 46) and the non-PDA group (n = 61).RESULTSThere were no significant differences in the distributions of the genotypes and allele frequencies of all studied SNP between the PDA group (n = 46) and the non-PDA group (n = 61).There were no significant associations between the studied SNP and the incidence of PDA in Japanese preterm infants. These SNP may not be clinically important predisposing factors for PDA in Japanese preterm infants.CONCLUSIONSThere were no significant associations between the studied SNP and the incidence of PDA in Japanese preterm infants. These SNP may not be clinically important predisposing factors for PDA in Japanese preterm infants. Persistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes, including angiotensin II receptor, type 1 (AGTR1), transcription factor AP-2 beta (TFAP2B) and tumor necrosis factor receptor-associated factor 1 (TRAF1), have been reported to be associated with PDA in preterm infants. The aim of this study was to evaluate the relationships between PDA in preterm infants and polymorphisms in AGTR1, TFAP2B and TRAF1 in the Japanese population. The subjects consisted of 107 preterm infants with gestational age <32 weeks. Extremely low-birthweight infants were treated with prophylactic indomethacin during the first 24 h after birth. Five SNP, namely, rs5186 in AGTR1, rs987237 and rs6930924 in TFAP2B, and rs1056567 and rs10985070 in TRAF1, were genotyped using TaqMan SNP genotyping assays. There were no significant differences in the distributions of the genotypes and allele frequencies of all studied SNP between the PDA group (n = 46) and the non-PDA group (n = 61). There were no significant associations between the studied SNP and the incidence of PDA in Japanese preterm infants. These SNP may not be clinically important predisposing factors for PDA in Japanese preterm infants. Background Persistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes, including angiotensin II receptor, type 1 (AGTR1), transcription factor AP‐2 beta (TFAP2B) and tumor necrosis factor receptor‐associated factor 1 (TRAF1), have been reported to be associated with PDA in preterm infants. The aim of this study was to evaluate the relationships between PDA in preterm infants and polymorphisms in AGTR1, TFAP2B and TRAF1 in the Japanese population. Methods The subjects consisted of 107 preterm infants with gestational age <32 weeks. Extremely low‐birthweight infants were treated with prophylactic indomethacin during the first 24 h after birth. Five SNP, namely, rs5186 in AGTR1, rs987237 and rs6930924 in TFAP2B, and rs1056567 and rs10985070 in TRAF1, were genotyped using TaqMan SNP genotyping assays. Results There were no significant differences in the distributions of the genotypes and allele frequencies of all studied SNP between the PDA group (n = 46) and the non‐PDA group (n = 61). Conclusions There were no significant associations between the studied SNP and the incidence of PDA in Japanese preterm infants. These SNP may not be clinically important predisposing factors for PDA in Japanese preterm infants. |
Author | Togawa, Takao Kouwaki, Masanori Saitoh, Shinji Yamada, Takaharu Ito, Koichi Kato, Takenori Koyama, Norihisa Sugimoto, Mari Nagasaki, Rika Sugiura, Tokio Nagaya, Yoshiaki Kawase, Koya |
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Cites_doi | 10.1540/jsmr.46.77 10.1038/bmt.2012.244 10.1067/mpd.2000.106569 10.1291/hypres.27.551 10.1097/00005176-200502000-00019 10.1007/BF01957576 10.1002/14651858.CD000174.pub2 10.1016/S0022-3476(96)80123-5 10.1111/j.1440-1681.2003.03942.x 10.1152/physiolgenomics.00231.2005 10.1159/000358013 10.1371/journal.pone.0101502 10.1542/peds.2008-0313 10.1159/000262481 10.1542/peds.2005-1528 10.1159/000226602 10.1067/S0022-3476(03)00303-2 10.1182/blood-2006-11-058446 10.1111/j.1365-2567.2006.02499.x 10.1203/01.PDR.0000088016.67117.39 10.1073/pnas.0409852102 10.1136/fn.75.3.F183 10.4103/0974-2069.58313 |
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References | Bökenkamp R, DeRuiter MC, van Munsteren C, Gittenberger-de Groot AC. Insights into the pathogenesis and genetic background of patency of the ductus arteriosus. Neonatology 2010; 98: 6-17. Zhang B, Wang Z, Li T, Tsitsikov EN, Ding HF. NF-kappaB2 mutation targets TRAF1 to induce lymphomagenesis. Blood 2007; 110: 743-51. Yokoyama U, Minamisawa S, Ishikawa Y. Regulation of vascular tone and remodeling of the ductus arteriosus. J. Smooth Muscle Res. 2010; 46: 77-87. Dollberg S, Lusky A, Reichman B. Patent ductus arteriosus, indomethacin and necrotizing enterocolitis in very low birth weight infants: A population-based study. J. Pediatr. Gastroenterol. Nutr. 2005; 40: 184-8. Kanda Y. Investigation of the freely-available easy-to-use software "EZR" (Easy R) for medical statistics. Bone Marrow Transplant. 2013; 48: 452-8. Kluckow M, Evans N. Ductal shunting, high pulmonary blood flow, and pulmonary hemorrhage. J. Pediatr. 2000; 137: 68-72. Pagni E, Baragatti B, Scebba F, Coceani F. Functional closure of the ductus arteriosus at birth: Evidence against an intermediary role of angiotensin II. Pharmacology 2014; 93: 120-5. Treszl A, Szabo M, Dunai G et al. Angiotensin II type 1 receptor A1166C polymorphism and prophylactic indomethacin treatment induced ductus arteriosus closure in very low birth weight neonates. Pediatr. Res. 2003; 54: 753-5. Mosalli R, Alfaleh K, Paes B. Role of prophylactic surgical ligation of patent ductus arteriosus in extremely low birth weight infants: Systematic review and implications for clinical practice. Ann. Pediatr. Cardiol. 2009; 2: 120-6. Oyoshi MK, Barthel R, Tsitsikov EN. TRAF1 regulates recruitment of lymphocytes and, to a lesser extent, neutrophils, myeloid dendritic cells and monocytes to the lung airways following lipopolysaccharide inhalation. Immunology 2007; 120: 303-14. Chan V, Greenough A, Gamsu HR. Neonatal complications of extreme prematurity in mechanically ventilated infants. Eur. J. Pediatr. 1992; 151: 693-6. Sugimoto K, Katsuya T, Ohkubo T et al. Association between angiotensin II type 1 receptor gene polymorphism and essential hypertension: The Ohasama Study. Hypertens. Res. 2004; 27: 551-6. Mani A, Radhakrishnan J, Farhi A et al. Syndromic patent ductus arteriosus: Evidence for haploinsufficient TFAP2B mutations and identification of a linked sleep disorder. Proc. Natl. Acad. Sci. USA. 2005; 102: 2975-9. Zhao F, Bosserhoff AK, Buettner R, Moser M. A heart-hand syndrome gene: TFAP2B plays a critical role in the development and remodeling of mouse ductus arteriosus and limb patterning. PLoS One 2011; 6: e22908. Costa M, Barogi S, Socci ND et al. Gene expression in ductus arteriosus and aorta: Comparison of birth and oxygen effects. Physiol. Genomics 2006; 25: 250-62. Koch J, Hensley G, Roy L, Brown S, Ramaciotti C, Rosenfeld CR. Prevalence of spontaneous closure of the ductus arteriosus in neonates at a birth weight of 1000 grams or less. Pediatrics 2006; 117: 1113-21. Clyman RI. Recommendations for the postnatal use of indomethacin: An analysis of four separate treatment strategies. J. Pediatr. 1996; 128: 601-7. Zhu YC, Zhu YZ, Lu N, Wang MJ, Wang YX, Yao T. Role of angiotensin AT1 and AT2 receptors in cardiac hypertrophy and cardiac remodelling. Clin. Exp. Pharmacol. Physiol. 2003; 30: 911-8. Evans N, Kluckow M. Early ductal shunting and intraventricular haemorrhage in ventilated preterm infants. Arch. Dis. Child. Fetal Neonatal Ed. 1996; 75: F183-6. Dagle JM, Lepp NT, Cooper ME et al. Determination of genetic predisposition to patent ductus arteriosus in preterm infants. Pediatrics 2009; 123: 1116-23. Chandra S, Narang R, Sreenivas V, Bhatia J, Saluja D, Srivastava K. Association of angiotensin II type 1 receptor (A1166C) gene polymorphism and its increased expression in essential hypertension: A case-control study. PLoS One 2014; 9: e101502. Spiegler J, Gilhaus A, Konig IR et al. Polymorphisms in the renin-angiotensin system and outcome of very-low-birthweight infants. Neonatology 2010; 97: 10-4. Fowlie PW, Davis PG, McGuire W. Prophylactic intravenous indomethacin for preventing mortality and morbidity in preterm infants. Cochrane Database Syst. Rev. 2010; (7): CD000174. Itabashi K, Ohno T, Nishida H. Indomethacin responsiveness of patent ductus arteriosus and renal abnormalities in preterm infants treated with indomethacin. J. Pediatr. 2003; 143: 203-7. 2010; 98 2010; 97 2013; 48 1992; 151 2010; 46 2000; 137 2004; 27 2005; 102 2007; 110 2006; 25 2007; 120 2005; 40 2009; 123 2014; 9 2009; 2 2011; 6 2006; 117 2003; 30 2014; 93 2010; 7 1996; 75 2003; 143 2003; 54 1996; 128 e_1_2_7_6_1 e_1_2_7_5_1 e_1_2_7_4_1 e_1_2_7_3_1 e_1_2_7_9_1 e_1_2_7_8_1 Zhao F (e_1_2_7_22_1) 2011; 6 e_1_2_7_7_1 e_1_2_7_19_1 e_1_2_7_18_1 e_1_2_7_17_1 e_1_2_7_16_1 e_1_2_7_2_1 e_1_2_7_15_1 e_1_2_7_14_1 e_1_2_7_25_1 e_1_2_7_13_1 e_1_2_7_24_1 e_1_2_7_12_1 e_1_2_7_23_1 e_1_2_7_11_1 e_1_2_7_10_1 e_1_2_7_21_1 e_1_2_7_20_1 |
References_xml | – reference: Kluckow M, Evans N. Ductal shunting, high pulmonary blood flow, and pulmonary hemorrhage. J. Pediatr. 2000; 137: 68-72. – reference: Mosalli R, Alfaleh K, Paes B. Role of prophylactic surgical ligation of patent ductus arteriosus in extremely low birth weight infants: Systematic review and implications for clinical practice. Ann. Pediatr. Cardiol. 2009; 2: 120-6. – reference: Treszl A, Szabo M, Dunai G et al. Angiotensin II type 1 receptor A1166C polymorphism and prophylactic indomethacin treatment induced ductus arteriosus closure in very low birth weight neonates. Pediatr. Res. 2003; 54: 753-5. – reference: Dagle JM, Lepp NT, Cooper ME et al. Determination of genetic predisposition to patent ductus arteriosus in preterm infants. Pediatrics 2009; 123: 1116-23. – reference: Bökenkamp R, DeRuiter MC, van Munsteren C, Gittenberger-de Groot AC. Insights into the pathogenesis and genetic background of patency of the ductus arteriosus. Neonatology 2010; 98: 6-17. – reference: Oyoshi MK, Barthel R, Tsitsikov EN. TRAF1 regulates recruitment of lymphocytes and, to a lesser extent, neutrophils, myeloid dendritic cells and monocytes to the lung airways following lipopolysaccharide inhalation. Immunology 2007; 120: 303-14. – reference: Fowlie PW, Davis PG, McGuire W. Prophylactic intravenous indomethacin for preventing mortality and morbidity in preterm infants. Cochrane Database Syst. Rev. 2010; (7): CD000174. – reference: Zhao F, Bosserhoff AK, Buettner R, Moser M. A heart-hand syndrome gene: TFAP2B plays a critical role in the development and remodeling of mouse ductus arteriosus and limb patterning. PLoS One 2011; 6: e22908. – reference: Spiegler J, Gilhaus A, Konig IR et al. Polymorphisms in the renin-angiotensin system and outcome of very-low-birthweight infants. Neonatology 2010; 97: 10-4. – reference: Mani A, Radhakrishnan J, Farhi A et al. Syndromic patent ductus arteriosus: Evidence for haploinsufficient TFAP2B mutations and identification of a linked sleep disorder. Proc. Natl. Acad. Sci. USA. 2005; 102: 2975-9. – reference: Clyman RI. Recommendations for the postnatal use of indomethacin: An analysis of four separate treatment strategies. J. Pediatr. 1996; 128: 601-7. – reference: Costa M, Barogi S, Socci ND et al. Gene expression in ductus arteriosus and aorta: Comparison of birth and oxygen effects. Physiol. Genomics 2006; 25: 250-62. – reference: Koch J, Hensley G, Roy L, Brown S, Ramaciotti C, Rosenfeld CR. Prevalence of spontaneous closure of the ductus arteriosus in neonates at a birth weight of 1000 grams or less. Pediatrics 2006; 117: 1113-21. – reference: Pagni E, Baragatti B, Scebba F, Coceani F. Functional closure of the ductus arteriosus at birth: Evidence against an intermediary role of angiotensin II. Pharmacology 2014; 93: 120-5. – reference: Evans N, Kluckow M. Early ductal shunting and intraventricular haemorrhage in ventilated preterm infants. Arch. Dis. Child. Fetal Neonatal Ed. 1996; 75: F183-6. – reference: Chan V, Greenough A, Gamsu HR. Neonatal complications of extreme prematurity in mechanically ventilated infants. Eur. J. Pediatr. 1992; 151: 693-6. – reference: Dollberg S, Lusky A, Reichman B. Patent ductus arteriosus, indomethacin and necrotizing enterocolitis in very low birth weight infants: A population-based study. J. Pediatr. Gastroenterol. Nutr. 2005; 40: 184-8. – reference: Yokoyama U, Minamisawa S, Ishikawa Y. Regulation of vascular tone and remodeling of the ductus arteriosus. J. Smooth Muscle Res. 2010; 46: 77-87. – reference: Sugimoto K, Katsuya T, Ohkubo T et al. Association between angiotensin II type 1 receptor gene polymorphism and essential hypertension: The Ohasama Study. Hypertens. Res. 2004; 27: 551-6. – reference: Chandra S, Narang R, Sreenivas V, Bhatia J, Saluja D, Srivastava K. Association of angiotensin II type 1 receptor (A1166C) gene polymorphism and its increased expression in essential hypertension: A case-control study. PLoS One 2014; 9: e101502. – reference: Kanda Y. Investigation of the freely-available easy-to-use software "EZR" (Easy R) for medical statistics. Bone Marrow Transplant. 2013; 48: 452-8. – reference: Itabashi K, Ohno T, Nishida H. Indomethacin responsiveness of patent ductus arteriosus and renal abnormalities in preterm infants treated with indomethacin. J. Pediatr. 2003; 143: 203-7. – reference: Zhu YC, Zhu YZ, Lu N, Wang MJ, Wang YX, Yao T. Role of angiotensin AT1 and AT2 receptors in cardiac hypertrophy and cardiac remodelling. Clin. Exp. Pharmacol. Physiol. 2003; 30: 911-8. – reference: Zhang B, Wang Z, Li T, Tsitsikov EN, Ding HF. NF-kappaB2 mutation targets TRAF1 to induce lymphomagenesis. Blood 2007; 110: 743-51. – volume: 137 start-page: 68 year: 2000 end-page: 72 article-title: Ductal shunting, high pulmonary blood flow, and pulmonary hemorrhage publication-title: J. Pediatr. – volume: 128 start-page: 601 year: 1996 end-page: 7 article-title: Recommendations for the postnatal use of indomethacin: An analysis of four separate treatment strategies publication-title: J. Pediatr. – volume: 117 start-page: 1113 year: 2006 end-page: 21 article-title: Prevalence of spontaneous closure of the ductus arteriosus in neonates at a birth weight of 1000 grams or less publication-title: Pediatrics – volume: 25 start-page: 250 year: 2006 end-page: 62 article-title: Gene expression in ductus arteriosus and aorta: Comparison of birth and oxygen effects publication-title: Physiol. Genomics – volume: 40 start-page: 184 year: 2005 end-page: 8 article-title: Patent ductus arteriosus, indomethacin and necrotizing enterocolitis in very low birth weight infants: A population‐based study publication-title: J. Pediatr. Gastroenterol. Nutr. – volume: 93 start-page: 120 year: 2014 end-page: 5 article-title: Functional closure of the ductus arteriosus at birth: Evidence against an intermediary role of angiotensin II publication-title: Pharmacology – volume: 7 year: 2010 article-title: Prophylactic intravenous indomethacin for preventing mortality and morbidity in preterm infants publication-title: Cochrane Database Syst. Rev. – volume: 123 start-page: 1116 year: 2009 end-page: 23 article-title: Determination of genetic predisposition to patent ductus arteriosus in preterm infants publication-title: Pediatrics – volume: 2 start-page: 120 year: 2009 end-page: 6 article-title: Role of prophylactic surgical ligation of patent ductus arteriosus in extremely low birth weight infants: Systematic review and implications for clinical practice publication-title: Ann. Pediatr. Cardiol. – volume: 46 start-page: 77 year: 2010 end-page: 87 article-title: Regulation of vascular tone and remodeling of the ductus arteriosus publication-title: J. Smooth Muscle Res. – volume: 110 start-page: 743 year: 2007 end-page: 51 article-title: NF‐kappaB2 mutation targets TRAF1 to induce lymphomagenesis publication-title: Blood – volume: 120 start-page: 303 year: 2007 end-page: 14 article-title: TRAF1 regulates recruitment of lymphocytes and, to a lesser extent, neutrophils, myeloid dendritic cells and monocytes to the lung airways following lipopolysaccharide inhalation publication-title: Immunology – volume: 97 start-page: 10 year: 2010 end-page: 4 article-title: Polymorphisms in the renin‐angiotensin system and outcome of very‐low‐birthweight infants publication-title: Neonatology – volume: 75 start-page: F183 year: 1996 end-page: 6 article-title: Early ductal shunting and intraventricular haemorrhage in ventilated preterm infants publication-title: Arch. Dis. Child. Fetal Neonatal Ed. – volume: 48 start-page: 452 year: 2013 end-page: 8 article-title: Investigation of the freely‐available easy‐to‐use software “EZR” (Easy R) for medical statistics publication-title: Bone Marrow Transplant. – volume: 143 start-page: 203 year: 2003 end-page: 7 article-title: Indomethacin responsiveness of patent ductus arteriosus and renal abnormalities in preterm infants treated with indomethacin publication-title: J. Pediatr. – volume: 151 start-page: 693 year: 1992 end-page: 6 article-title: Neonatal complications of extreme prematurity in mechanically ventilated infants publication-title: Eur. J. Pediatr. – volume: 6 year: 2011 article-title: A heart‐hand syndrome gene: TFAP2B plays a critical role in the development and remodeling of mouse ductus arteriosus and limb patterning publication-title: PLoS One – volume: 9 year: 2014 article-title: Association of angiotensin II type 1 receptor (A1166C) gene polymorphism and its increased expression in essential hypertension: A case–control study publication-title: PLoS One – volume: 27 start-page: 551 year: 2004 end-page: 6 article-title: Association between angiotensin II type 1 receptor gene polymorphism and essential hypertension: The Ohasama Study publication-title: Hypertens. Res. – volume: 98 start-page: 6 year: 2010 end-page: 17 article-title: Insights into the pathogenesis and genetic background of patency of the ductus arteriosus publication-title: Neonatology – volume: 102 start-page: 2975 year: 2005 end-page: 9 article-title: Syndromic patent ductus arteriosus: Evidence for haploinsufficient TFAP2B mutations and identification of a linked sleep disorder publication-title: Proc. Natl. Acad. Sci. USA. – volume: 30 start-page: 911 year: 2003 end-page: 8 article-title: Role of angiotensin AT1 and AT2 receptors in cardiac hypertrophy and cardiac remodelling publication-title: Clin. Exp. Pharmacol. Physiol. – volume: 54 start-page: 753 year: 2003 end-page: 5 article-title: Angiotensin II type 1 receptor A1166C polymorphism and prophylactic indomethacin treatment induced ductus arteriosus closure in very low birth weight neonates publication-title: Pediatr. Res. – ident: e_1_2_7_17_1 doi: 10.1540/jsmr.46.77 – ident: e_1_2_7_14_1 doi: 10.1038/bmt.2012.244 – ident: e_1_2_7_2_1 doi: 10.1067/mpd.2000.106569 – ident: e_1_2_7_16_1 doi: 10.1291/hypres.27.551 – ident: e_1_2_7_4_1 doi: 10.1097/00005176-200502000-00019 – ident: e_1_2_7_3_1 doi: 10.1007/BF01957576 – ident: e_1_2_7_6_1 doi: 10.1002/14651858.CD000174.pub2 – ident: e_1_2_7_9_1 doi: 10.1016/S0022-3476(96)80123-5 – ident: e_1_2_7_20_1 doi: 10.1111/j.1440-1681.2003.03942.x – ident: e_1_2_7_18_1 doi: 10.1152/physiolgenomics.00231.2005 – ident: e_1_2_7_21_1 doi: 10.1159/000358013 – volume: 6 year: 2011 ident: e_1_2_7_22_1 article-title: A heart‐hand syndrome gene: TFAP2B plays a critical role in the development and remodeling of mouse ductus arteriosus and limb patterning publication-title: PLoS One – ident: e_1_2_7_15_1 doi: 10.1371/journal.pone.0101502 – ident: e_1_2_7_12_1 doi: 10.1542/peds.2008-0313 – ident: e_1_2_7_19_1 doi: 10.1159/000262481 – ident: e_1_2_7_7_1 doi: 10.1542/peds.2005-1528 – ident: e_1_2_7_13_1 doi: 10.1159/000226602 – ident: e_1_2_7_8_1 doi: 10.1067/S0022-3476(03)00303-2 – ident: e_1_2_7_24_1 doi: 10.1182/blood-2006-11-058446 – ident: e_1_2_7_25_1 doi: 10.1111/j.1365-2567.2006.02499.x – ident: e_1_2_7_11_1 doi: 10.1203/01.PDR.0000088016.67117.39 – ident: e_1_2_7_23_1 doi: 10.1073/pnas.0409852102 – ident: e_1_2_7_5_1 doi: 10.1136/fn.75.3.F183 – ident: e_1_2_7_10_1 doi: 10.4103/0974-2069.58313 |
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Persistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes,... Persistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes, including... Background Persistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes,... BackgroundPersistent patent ductus arteriosus (PDA) is a frequent complication in preterm infants. Single nucleotide polymorphisms (SNP) in several genes,... |
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SubjectTerms | Angiotensin Angiotensin II AP-2 protein Babies Baby foods Birth weight Congenital diseases Coronary vessels DNA - genetics Ductus Arteriosus, Patent - epidemiology Ductus Arteriosus, Patent - genetics Ductus Arteriosus, Patent - metabolism Female Gene frequency Genes Genotype Genotyping Gestational Age Humans Incidence Indomethacin Infant, Extremely Low Birth Weight Infant, Newborn Infant, Premature Infants Japan - epidemiology Male Newborn babies patent ductus arteriosus Pediatrics Polymorphism Polymorphism, Single Nucleotide Premature babies Premature birth preterm infant Receptor, Angiotensin, Type 1 - genetics Receptor, Angiotensin, Type 1 - metabolism Respiratory therapy Single-nucleotide polymorphism TNF Receptor-Associated Factor 1 - genetics TNF Receptor-Associated Factor 1 - metabolism Transcription Factor AP-2 - genetics Transcription Factor AP-2 - metabolism |
Title | Single nucleotide polymorphisms in AGTR1, TFAP2B, and TRAF1 are not associated with the incidence of patent ductus arteriosus in Japanese preterm infants |
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