Polymorphisms of Placental Iodothyronine Deiodinase Genes in a Rural Area of Northern China with High Prevalence of Neural Tube Defects.

Introduction: We have reported that high total homocysteine and the coexistence of inadequate thyroid hormones in maternal serum increase the risk of fetal neural tube defects (NTDs). Placental iodothyronine deiodinases (DIOs: DIO1, DIO2, and DIO3) play a role in regulating the conversions between different forms of maternal thyroid hormones. This study hypothesized that single nucleotide polymorphisms (SNPs) in placental DIOs genes could be related to NTDs.

Higher serum homocysteine and lower thyroid hormone levels in pregnant women are associated with neural tube defects.

Background: This study tested the hypothesis that abnormal maternal metabolism of both homocysteine and thyroid hormone network in pregnant women is associated with neural tube defects (NTDs) in a part of China with high NTD prevalence.

Methods: A case-control study was performed between 2007 and 2009 in Lüliang Mountains, Shanxi Province. This study included 83 pregnant women who had fetuses with NTDs (cases) and 90 pregnant women with normal fetuses (controls).

Genetic screening and functional analysis of CASP9 mutations in a Chinese cohort with neural tube defects.

Aim: Neural tube defects (NTDs) are birth defects of the nervous system and are the second most frequent cause of birth defects worldwide. The etiology of NTDs is complicated and involves both genetic and environmental factors. CASP9 is an initiator caspase in the intrinsic apoptosis pathway, which in Casp9 mice has been shown to result in NTDs because of decreased apoptosis.

Sonic Hedgehog Signaling Affected by Promoter Hypermethylation Induces Aberrant Gli2 Expression in Spina Bifida.

GLI2 is a key mediator of the sonic hedgehog (Shh) signaling pathway and plays an important role in neural tube development during vertebrate embryogenesis; however, the role of gli2 in human folate-related neural tube defects remains unclear. In this study, we compared methylation status and polymorphisms of gli2 between spina bifida patients and a control group to explore the underlying mechanisms related to folate deficiency in spina bifida. No single nucleotide polymorphism was found to be significantly different between the two groups, although gli2 methylation levels were significantly increased in spina bifida samples, accompanied by aberrant GLI2 expression.

[Recombinant expression of human influenza A virus nucleocapsid protein and its antigenicity analyses].

Objective: To prepare anti-recombinant protein antibody from immunized mice with recombinant nucleocapsid protein (NP) of human influenza A3 (IFV-A3) virus expressed in prokaryotic cell, and to explore the feasibility of utilizing anti-recombinant protein antibody to detect influenza A virus.

Methods: NP genes of human influenza A virus were analyzed with computer softwares of ClustalX, Antheprot, et al. to determine the antigenicity in conserved regions.