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hypothyroidism/ニコチン

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Effect of chronic stress or nicotine on hypothyroidism-induced enhancement of LTD: electrophysiological and molecular studies.

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We have shown recently that either hypothyroidism or chronic psychosocial stress enhances the expression of LTD, which is reversed by chronic nicotine treatment. In this study, we investigated the effect of combining chronic psychosocial stress with hypothyroidism on LTD. We have also investigated

High occurrence of thyroid multinodularity and low occurrence of subclinical hypothyroidism among tobacco smokers in a large population study.

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Tobacco smoking increases the risk of goitre and Graves' disease, but the association with thyroid nodularity and hypothyroidism has not been settled. We investigated 4649 subjects from the general population with questionnaires, thyroid ultrasonography and blood tests. The results were analysed in

Comparison of Effects of Spatial and Non-Spatial Memory Acquisition on the CaMKII Pathway During Hypothyroidism and Nicotine Treatment.

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Molecular, cellular, and behavioral studies have shown that hypothyroidism impairs hippocampus-dependent learning and memory in adult rats. In these studies, spatial learning and memory were tested in the radial arm water maze (RAWM), which involved locating a hidden platform. In the present study,

Nicotine prevents disruption of the late phase LTP-related molecular cascade in adult-onset hypothyroidism.

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We have shown previously that chronic nicotine treatment reverses adult-onset hypothyroidism-induced impairment of late-phase long-term potentiation (L-LTP) in area CA1 of the hippocampus. In the present study, basal and stimulated levels of signaling molecules essential for the expression of L-LTP

Chronic nicotine treatment reverses hypothyroidism-induced impairment of L-LTP induction phase: critical role of CREB.

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We have previously shown that adult onset hypothyroidism impairs late-phase long-term potentiation (L-LTP) and reduces basal protein levels of cyclic-AMP response element binding protein (CREB), mutagen-activated protein kinase (MAPKp42/44), and calcium calmodulin kinase IV (CaMKIV) in area Cornu

Nicotine reverses adult-onset hypothyroidism-induced impairment of learning and memory: Behavioral and electrophysiological studies.

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Nicotine alleviates cognitive impairment associated with a variety of health conditions. We examined the effect of chronic nicotine treatment on adult-onset hypothyroidism-induced impairment of learning and memory in rats. Hypothyroidism was induced by surgical removal of thyroid glands

Neonatal hypothyroidism caused by maternal nicotine exposure is reversed by higher T3 transfer by milk after nicotine withdraw.

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Maternal nicotine exposure leads to neonatal hypothyroidism that can be returned to euthyroidism after nicotine withdrawal. Here, we examined the transfer of iodine through milk, deiodinase activities (D1 and D2), and serum T3, T4 and TSH in rat offspring after maternal exposure to nicotine. One day

Molecular studies on the protective effect of nicotine in adult-onset hypothyroidism-induced impairment of long-term potentiation.

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We have recently shown that chronic nicotine treatment reverses hypothyroidism-induced learning and memory impairment. Chronic nicotine treatment also reverses the hypothyroidism-induced impairment of long-term potentiation (LTP). Analysis of LTP associated key signaling molecules revealed that
The Bienenstock, Cooper, and Munro (BCM) theory or the sliding threshold model can be used to explain the changes in synaptic plasticity related to learning and memory, namely long-term potentiation (LTP) and depression (LTD). In this study, we applied synaptic plasticity changes induced by either

Adult-onset hypothyroidism facilitates and enhances LTD: reversal by chronic nicotine treatment.

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Chronic nicotine treatment reverses hypothyroidism-induced impairment of hippocampus-dependent spatial memory and long-term potentiation (LTP). We investigated the effect of hypothyroidism on long-term depression (LTD) and possible protection by nicotine. Following paired pulse stimulation, LTD was
Although autoimmune hypothyroidism has generally been considered to be a disease that mainly develops because of genetic aberrations and for which adjustment of environment would bring about but slight risk modification, this understanding is increasingly appearing to be incorrect. We describe how

Warthin's tumour associated with autoimmune diseases and tobacco use.

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To better clarify the possible role of immune mechanisms in the pathogenesis of Warthin's tumour (WT), we performed a retrospective study of patients with WT surgically treated at the Institute of Otolaryngology Head and Neck Surgery, University of Florence, during a 25-year period; looking for a
Epidemiological studies show a higher prevalence of obesity in children from smoking mothers and smoking may affect human thyroid function. To evaluate the mechanism of smoking as an imprinting factor for these dysfunctions, we evaluated the programming effects of maternal nicotine (NIC) exposure

The effect of nicotine on thyroid function in rats.

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Very recently, it has been reported that subclinical hypothyroidism is more severe and peripheral markers of hypothyroidism are more pronounced in women with subclinical or overt hypothyroidism who smoke. Increased concentrations of the known goitrogen thiocyanate, generated from cigarette smoke,
OBJECTIVE Postnatal nicotine exposure causes precocious primary hypothyroidism and programs for overweight, hyperleptinemia and secondary hypothyroidism in adulthood. As leptin and thyroid hormones share the ability to increase energy expenditure, we studied the effects of maternal nicotine exposure
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