10 Papers
82 Citations
Qi Xi is an academic researcher from University of Tennessee Health Science Center. The author has contributed to research in topics: Offspring & Iodine deficiency. The author has an hindex of 7, co-authored 10 publications. Previous affiliations of Qi Xi include China Medical University (PRC).
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Papers
Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny
TL;DR: R rodent models provide direct evidence of neurodevelopmental damage induced by maternal hypothyroxinemia, including dendritic and axonal growth limitation, neural abnormal location, and synaptic function alteration, which suggest an independent role of T4.
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Developmental iodine deficiency and hypothyroidism impair neural development in rat hippocampus: involvement of doublecortin and NCAM-180.
Jian Gong,Wanyang Liu,Jing Dong,Yi Wang,Hongde Xu,Wei Wei,Jiapeng Zhong,Qi Xi,Qi Xi,Jie Chen +9 more
TL;DR: Developmental iodine deficiency and hypothyroidism impair the expression of doublecortin and NCAM-180, leading to nerve fiber malfunction and thus impairments in hippocampal development.
Developmental Hypothyroxinaemia Induced by Maternal Mild Iodine Deficiency Delays Hippocampal Axonal Growth in the Rat Offspring
TL;DR: The hypothesis that maternal hypothyroxinaemia may impair axonal growth of the offspring is supported by the results, which showed that mothers with mild iodine deficiency exposure delayed offspring axonal Growth Delay.
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Marginal Iodine Deficiency Affects Dendritic Spine Development by Disturbing the Function of Rac1 Signaling Pathway on Cytoskeleton
TL;DR: This study may support the hypothesis that decreased T4 induced by marginal ID results in slight impairments of LTP and leads to mild damage of dendritic spine development, which may be due to abnormal regulation of Rac1 signaling pathway on cytoskeleton.
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Effects of Maternal Marginal Iodine Deficiency on Dendritic Morphology in the Hippocampal CA1 Pyramidal Neurons in Rat Offspring.
TL;DR: It is speculated that the pups treated with maternal marginal ID subjected to subtle changes in dendritic growth of CA1 pyramidal neurons, which may be associated with the dysregulation of MAP2 and stathmin in a JNK1-dependent manner.
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