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“Diversity of endophytic fungi of Myricaria laxiflora grown under pre- and post-flooding conditions”, vol. 14, pp. 10849-10862, 2015.
, “A66G and C524T polymorphisms of the methionine synthase reductase gene are associated with congenital heart defects in the Chinese Han population”, vol. 10, pp. 2597-2605, 2011.
, Berry RJ, Li Z, Erickson JD, Li S, et al. (1999). Prevention of neural-tube defects with folic acid in China. China-U.S. Collaborative Project for Neural Tube Defect Prevention. N. Engl. J. Med. 341: 1485-1490.
http://dx.doi.org/10.1056/NEJM199911113412001
PMid:10559448
Botto LD and Correa A (2003). Decreasing the burden of congenital heart anomalies: an epidemiologic evaluation of risk factors and survival. Prog. Pediatr. Cardiol. 18: 111-121.
http://dx.doi.org/10.1016/S1058-9813(03)00084-5
Botto LD, Khoury MJ, Mulinare J and Erickson JD (1996). Periconceptional multivitamin use and the occurrence of conotruncal heart defects: results from a population-based, case-control study. Pediatrics 98: 911-917.
PMid:8909485
Botto LD, Mulinare J and Erickson JD (2000). Occurrence of congenital heart defects in relation to maternal mulitivitamin use. Am. J. Epidemiol. 151: 878-884.
PMid:10791560
Botto LD, Mulinare J and Erickson JD (2003). Do multivitamin or folic acid supplements reduce the risk for congenital heart defects? Evidence and gaps. Am. J. Med. Genet. A 121A: 95-101.
http://dx.doi.org/10.1002/ajmg.a.20132
PMid:12910485
Botto LD, Olney RS and Erickson JD (2004). Vitamin supplements and the risk for congenital anomalies other than neural tube defects. Am. J. Med. Genet. C. Semin. Med. Genet. 125C: 12-21.
http://dx.doi.org/10.1002/ajmg.c.30004
PMid:14755429
Brookes AJ (1999). The essence of SNPs. Gene 234: 177-186.
http://dx.doi.org/10.1016/S0378-1119(99)00219-X
Czeizel AE (1998). Periconceptional folic acid containing multivitamin supplementation. Eur. J. Obstet. Gynecol. Reprod. Biol. 78: 151-161.
http://dx.doi.org/10.1016/S0301-2115(98)00061-X
Czeizel AE and Dudás I (1992). Prevention of the first occurrence of neural-tube defects by periconceptional vitamin supplementation. N. Engl. J. Med. 327: 1832-1835.
http://dx.doi.org/10.1056/NEJM199212243272602
PMid:1307234
Czeizel AE, Dobo M and Vargha P (2004). Hungarian cohort-controlled trial of periconceptional multivitamin supplementation shows a reduction in certain congenital abnormalities. Birth Defects Res. A Clin. Mol. Teratol. 70: 853-861.
http://dx.doi.org/10.1002/bdra.20086
PMid:15523663
Deng L, Elmore CL, Lawrance AK, Matthews RG, et al. (2008). Methionine synthase reductase deficiency results in adverse reproductive outcomes and congenital heart defects in mice. Mol. Genet. Metab. 94: 336-342.
http://dx.doi.org/10.1016/j.ymgme.2008.03.004
PMid:18413293 PMCid:3110750
Elmore CL, Wu X, Leclerc D, Watson ED, et al. (2007). Metabolic derangement of methionine and folate metabolism in mice deficient in methionine synthase reductase. Mol. Genet. Metab. 91: 85-97.
http://dx.doi.org/10.1016/j.ymgme.2007.02.001
PMid:17369066 PMCid:1973089
Fredriksen A, Meyer K, Ueland PM, Vollset SE, et al. (2007). Large-scale population-based metabolic phenotyping of thirteen genetic polymorphisms related to one-carbon metabolism. Hum. Mutat. 28: 856-865.
http://dx.doi.org/10.1002/humu.20522
PMid:17436311
Gellekink H, den Heijer M, Heil SG and Blom HJ (2005). Genetic determinants of plasma total homocysteine. Semin. Vasc. Med. 5: 98-109.
http://dx.doi.org/10.1055/s-2005-872396
PMid:16047263
Hoffman JI and Kaplan S (2002). The incidence of congenital heart disease. J. Am. Coll. Cardiol. 39: 1890-1900.
http://dx.doi.org/10.1016/S0735-1097(02)01886-7
Huhta JC, Linask K and Bailey L (2006). Recent advances in the prevention of congenital heart disease. Curr. Opin. Pediatr. 18: 484-489.
http://dx.doi.org/10.1097/01.mop.0000245347.45336.d7
PMid:16969161
Itikala PR, Watkins ML, Mulinare J, Moore CA, et al. (2001). Maternal multivitamin use and orofacial clefts in offspring. Teratology 63: 79-86.
http://dx.doi.org/10.1002/1096-9926(200102)63:2<79::AID-TERA1013>3.0.CO;2-3
Kapusta L, Haagmans ML, Steegers EA, Cuypers MH, et al. (1999). Congenital heart defects and maternal derangement of homocysteine metabolism. J. Pediatr. 135: 773-774.
http://dx.doi.org/10.1016/S0022-3476(99)70102-2
Lai E (2001). Application of SNP technologies in medicine: lessons learned and future challenges. Genome Res. 11: 927- 929.
http://dx.doi.org/10.1101/gr.192301
PMid:11381021
Leclerc D, Odievre M, Wu Q, Wilson A, et al. (1999). Molecular cloning, expression and physical mapping of the human methionine synthase reductase gene. Gene 240: 75-88.
http://dx.doi.org/10.1016/S0378-1119(99)00431-X
Olteanu H and Banerjee R (2001). Human methionine synthase reductase, a soluble P-450 reductase-like dual flavoprotein, is sufficient for NADPH-dependent methionine synthase activation. J. Biol. Chem. 276: 35558-35563.
http://dx.doi.org/10.1074/jbc.M103707200
PMid:11466310
Rosenquist TH, Ratashak SA and Selhub J (1996). Homocysteine induces congenital defects of the heart and neural tube: effect of folic acid. Proc. Natl. Acad. Sci. U. S. A. 93: 15227-15232.
http://dx.doi.org/10.1073/pnas.93.26.15227
Shaw GM, Lu W, Zhu H, Yang W, et al. (2009). 118 SNPs of folate-related genes and risks of spina bifida and conotruncal heart defects. BMC Med. Genet. 10: 49.
http://dx.doi.org/10.1186/1471-2350-10-49
PMid:19493349 PMCid:2700092
Silaste ML, Rantala M, Sampi M, Alfthan G, et al. (2001). Polymorphisms of key enzymes in homocysteine metabolism affect diet responsiveness of plasma homocysteine in healthy women. J. Nutr. 131: 2643-2647.
PMid:11584084
Swanson DA, Liu ML, Baker PJ, Garrett L, et al. (2001). Targeted disruption of the methionine synthase gene in mice. Mol. Cell. Biol. 21: 1058-1065.
http://dx.doi.org/10.1128/MCB.21.4.1058-1065.2001
PMid:11158293 PMCid:99560
Tennstedt C, Chaoui R, Korner H and Dietel M (1999). Spectrum of congenital heart defects and extracardiac malformations associated with chromosomal abnormalities: results of a seven year necropsy study. Heart 82: 34-39.
PMid:10377306 PMCid:1729082
Tierney BJ, Ho T, Reedy MV and Brauer PR (2004). Homocysteine inhibits cardiac neural crest cell formation and morphogenesis in vivo. Dev. Dyn. 229: 63-73.
http://dx.doi.org/10.1002/dvdy.10469
PMid:14699578
van Beynum IM, Kouwenberg M, Kapusta L, den Heijer M, et al. (2006). MTRR 66A>G polymorphism in relation to congenital heart defects. Clin. Chem. Lab. Med. 44: 1317-1323.
http://dx.doi.org/10.1515/CCLM.2006.254
PMid:17087642
Verkleij-Hagoort AC, Verlinde M, Ursem NT, Lindemans J, et al. (2006). Maternal hyperhomocysteinaemia is a risk factor for congenital heart disease. BJOG 113: 1412-1418.
http://dx.doi.org/10.1111/j.1471-0528.2006.01109.x
Verkleij-Hagoort AC, van Driel LM, Lindemans J, Isaacs A, et al. (2008). Genetic and lifestyle factors related to the periconception vitamin B12 status and congenital heart defects: a dutch case-control study. Mol. Genet. Metab. 94: 112-119.
http://dx.doi.org/10.1016/j.ymgme.2007.12.002
PMid:18226574
“Zinc finger protein A20 overexpression inhibits monocyte homing and protects endothelial cells from injury induced by high glucose”, vol. 10, pp. 1050-1059, 2011.
, Fogelman AM, Elahi F, Sykes K, Van Lenten BJ, et al. (1988). Modification of the Recalde method for the isolation of human monocytes. J. Lipid Res. 29: 1243-1247.
PMid:3183529
La Fontaine J, Harkless LB, Davis CE, Allen MA, et al. (2006). Current concepts in diabetic microvascular dysfunction. J. Am. Podiatr. Med. Assoc. 96: 245-252.
PMid:16707637
Lutz J, Luong Le A, Strobl M, Deng M, et al. (2008). The A20 gene protects kidneys from ischaemia/reperfusion injury by suppressing pro-inflammatory activation. J. Mol. Med. 86: 1329-1339.
doi:10.1007/s00109-008-0405-4
PMid:18813897
McGinn S, Saad S, Poronnik P and Pollock CA (2003). High glucose-mediated effects on endothelial cell proliferation occur via p38 MAP kinase. Am. J. Physiol. Endocrinol. Metab. 285: E708-E717.
PMid:12783777
Mohan S, Mohan N, Valente AJ and Sprague EA (1999). Regulation of low shear flow-induced HAEC VCAM-1 expression and monocyte adhesion. Am. J. Physiol. 276: C1100-C1107.
PMid:10329958
Patel VI, Daniel S, Longo CR, Shrikhande GV, et al. (2006). A20, a modulator of smooth muscle cell proliferation and apoptosis, prevents and induces regression of neointimal hyperplasia. FASEB J. 20: 1418-1430.
doi:10.1096/fj.05-4981com
PMid:16816117
Romero MJ, Platt DH, Tawfik HE, Labazi M, et al. (2008). Diabetes-induced coronary vascular dysfunction involves increased arginase activity. Circ. Res. 102: 95-102.
doi:10.1161/CIRCRESAHA.107.155028
PMid:17967788 PMCid:2822539
Wang AB, Li HL, Zhang R, She ZG, et al. (2007). A20 attenuates vascular smooth muscle cell proliferation and migration through blocking PI3k/Akt singling in vitro and in vivo. J. Biomed. Sci. 14: 357-371.
doi:10.1007/s11373-007-9150-x
PMid:17260188
Yang WS, Seo JW, Han NJ, Choi J, et al. (2008). High glucose-induced NF-kappaB activation occurs via tyrosine phosphorylation of IkappaBalpha in human glomerular endothelial cells: involvement of Syk tyrosine kinase. Am. J. Physiol. Renal Physiol. 294: F1065-F1075.
doi:10.1152/ajprenal.00381.2007
PMid:18353872
Zeng W, Li L, Yuan W, Wei Y, et al. (2009). A20 overexpression inhibits low shear flow-induced CD14-positive monocyte recruitment to endothelial cells. Biorheology 46: 21-30.
PMid:19252225
Zhu CH, Ying DJ, Mi JH, Zhang W, et al. (2004). The zinc finger protein A20 protects endothelial cells from burns serum injury. Burns 30: 127-133.
doi:10.1016/j.burns.2003.08.010
PMid:15019119