Hypothyroidism and Brain Development

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Hypothyroidism and brain developmental players

Most of our knowledge on the mechanisms of thyroid hormone (TH) dependent brain development is based on clinical observations and animal studies of maternal/fetal hypothyroidism. THs play an essential role in brain development and hormone deficiency during critical phases in fetal life may lead to severe and permanent brain damage. Maternal hypothyroidism is considered the most common cause of ...

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congenital hypothyroidism: etiology and growth-development outcome.

one of the most preventable causes of mental and growth retardation is congenital hypothyroidism (ch). this study tries to investigate growth and mental outcome of patients with ch. since november 2006 and november 2007 in guilan province, north of iran, all neonates who were diagnosed with ch, evaluated for etiology of ch by laboratory follow up, thyroid sonography or scan. growth and developm...

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Hypothyroidism Enhances Tumor Invasiveness and Metastasis Development

BACKGROUND Whereas there is increasing evidence that loss of expression and/or function of the thyroid hormone receptors (TRs) could result in a selective advantage for tumor development, the relationship between thyroid hormone levels and human cancer is a controversial issue. It has been reported that hypothyroidism might be a possible risk factor for liver and breast cancer in humans, but a ...

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Neuronal Mitochondrial Morphology and Transmembrane Potential Are Severely Altered by Hypothyroidism during Rat Brain Development.

We recently demonstrated that thyroid hormone is an important regulator of mitochondrial gene expression during brain development. To gain further insights into the consequences of this regulation, we have performed functional and structural analysis of brain mitochondria from control and hypothyroid neonatal rats. Flow cytometric analysis showed a significant decrease in the mitochondrial tran...

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ژورنال

عنوان ژورنال: Journal of Animal Research and Nutrition

سال: 2017

ISSN: 2572-5459

DOI: 10.21767/2572-5459.100033