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10.1002/bdra.23483 http://scihub22266oqcxt.onion/10.1002/bdra.23483 C4801756!4801756!26900104     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Birth+Defects+Res+A+Clin+Mol+Teratol 2016 ; 106 (3): 201-7 Nephropedia Template TP {{tp|p=26900104|t=2016. Autoantibodies Against Homocysteinylated Protein in a Mouse Model of Folate Deficiency-Induced Neural Tube Defects |pdf=|usr=}}{{26900104}} gab.com Text Autoantibodies Against Homocysteinylated Protein in a Mouse Model of Folate Deficiency-Induced Neural Tube Defects JO: Birth Defects Res A Clin Mol Teratol http://www.kidney.de/pget.php?&tw=1&pmid=26900104 #FOAvip Periconceptional supplementation with folic acid results in a significant reduction in the incidence of neural tube defects (NTDs). Nonetheless, NTDs remain a leading cause of perinatal morbidity and mortality worldwide, and the mechanism(s) by which folate exerts its protective effects are unknown. Homocysteine is an amino acid that accumulates under conditions of folate-deficiency, and is suggested as a risk factor for NTDs. One proposed mechanism of homocysteine toxicity is its accumulation into proteins in a process termed homocysteinylation. Herein, we used a folate-deficient diet in pregnant mice to demonstrate that there is: (i) a significant inverse correlation between maternal serum folate levels and serum homocysteine; (ii) a significant positive correlation between serum homocysteine levels and titers of autoantibodies against homocysteinylated protein; and (iii) a significant increase in congenital malformations and NTDs in mice deficient in serum folate. Further, in mice administered the folate-deplete diet prior to conception, supplementation with folic acid during the gestational period completely rescued the embryos from congenital defects, and resulted in homocysteinylated protein titers at term that are comparable to that of mice administered a folate-replete diet throughout both the pre- and post-conception period. These results demonstrate that a low-folate diet that induces NTDs also increases protein homocysteinylation and the subsequent generation of autoantibodies against homocysteinylated proteins. These data support the hypotheses that homocysteinylation results in neo-self antigen formation under conditions of maternal folate deficiency, and that this process is reversible with folic acid supplementation. Twit Text FOAVip Autoantibodies Against Homocysteinylated Protein in a Mouse Model of Folate Deficiency-Induced Neural Tube Defects ????Birth Defects Res A Clin Mol Teratol http://www.kidney.de/pget.php?&tw=1&pmid=26900104 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26900104 #FOAvip English Wikipedia <ref>{{Cite pmid|26900104}}</ref> Autoantibodies Against Homocysteinylated Protein in a Mouse Model of Folate Deficiency-Induced Neural Tube Defects #MMPMID26900104 Denny K; Kelly C; Kumar V; Witham K; Cabrera R; Finnell R; Taylor S; Jeanes A; Woodruff T Birth Defects Res A Clin Mol Teratol 2016[Mar]; 106 (3): 201-7 PMID26900104show ga Periconceptional supplementation with folic acid results in a significant reduction in the incidence of neural tube defects (NTDs). Nonetheless, NTDs remain a leading cause of perinatal morbidity and mortality worldwide, and the mechanism(s) by which folate exerts its protective effects are unknown. Homocysteine is an amino acid that accumulates under conditions of folate-deficiency, and is suggested as a risk factor for NTDs. One proposed mechanism of homocysteine toxicity is its accumulation into proteins in a process termed homocysteinylation. Herein, we used a folate-deficient diet in pregnant mice to demonstrate that there is: (i) a significant inverse correlation between maternal serum folate levels and serum homocysteine; (ii) a significant positive correlation between serum homocysteine levels and titers of autoantibodies against homocysteinylated protein; and (iii) a significant increase in congenital malformations and NTDs in mice deficient in serum folate. Further, in mice administered the folate-deplete diet prior to conception, supplementation with folic acid during the gestational period completely rescued the embryos from congenital defects, and resulted in homocysteinylated protein titers at term that are comparable to that of mice administered a folate-replete diet throughout both the pre- and post-conception period. These results demonstrate that a low-folate diet that induces NTDs also increases protein homocysteinylation and the subsequent generation of autoantibodies against homocysteinylated proteins. These data support the hypotheses that homocysteinylation results in neo-self antigen formation under conditions of maternal folate deficiency, and that this process is reversible with folic acid supplementation. äAutoantibodies Against Homocysteinylated Protein in a Mouse Model of F(epmc).pdf DeepDyve Pubget Overpricing