scholarly journals Tissue Distribution of 125I-Labeled Fetal Thyroid Hormone in Nude Mice Xenografted with Ewing Sarcoma.

1992 ◽  
Vol 167 (3) ◽  
pp. 239-242
Author(s):  
MASAHITO HATORI ◽  
JOSEPH P. DUTKOWSKY ◽  
RICHARD A. SMITH ◽  
ROBERT S. WILLIAMS ◽  
TAKASHI YOKOTA ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Tissue Distribution ◽  
Nude Mice ◽  
Ewing Sarcoma ◽  
Fetal Thyroid

scholarly journals Placental 5-Deiodinase Activity and Fetal Thyroid Hormone Economy Are Unaffected by Selenium Deficiency in the Rat

1993 ◽  
Vol 34 (3) ◽  
pp. 288-292 ◽  
Author(s):  
Jean-Pierre Chanoine ◽  
Sharon Alex ◽  
Scott Stone ◽  
Shih Lieh Fang ◽  
Irini Veronikis ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Selenium Deficiency ◽  
Deiodinase Activity ◽  
Fetal Thyroid

scholarly journals Thyroid Hormone Deficiency Before the Onset of Hearing Causes Irreversible Damage to Peripheral and Central Auditory Systems

2000 ◽  
Vol 83 (5) ◽  
pp. 3101-3112 ◽  
Author(s):  
Marlies Knipper ◽  
Christoph Zinn ◽  
Hannes Maier ◽  
Mark Praetorius ◽  
Karin Rohbock ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Gland ◽  
Auditory System ◽  
Critical Time ◽  
Organ Of Corti ◽  
Thyroid Gland Function ◽  
Distortion Product ◽  
Fetal Thyroid ◽  
Gland Function ◽  
Dependent Processes

Both a genetic or acquired neonatal thyroid hormone (TH) deficiency may result in a profound mental disability that is often accompanied by deafness. The existence of various TH-sensitive periods during inner ear development and general success of delayed, corrective TH treatment was investigated by treating pregnant and lactating rats with the goitrogen methimazole (MMI). We observed that for the establishment of normal hearing ability, maternal TH, before fetal thyroid gland function on estrus days 17–18, is obviously not required. Within a crucial time between the onset of fetal thyroid gland function and the onset of hearing at postnatal day 12 ( P12), any postponement in the rise of TH-plasma levels, as can be brought about by treating lactating mothers with MMI, leads to permanent hearing defects of the adult offspring. The severity of hearing defects that were measured in 3- to 9-mo-old offspring could be increased with each additional day of TH deficiency during this critical period. Unexpectedly, the active cochlear process, assayed by distortion product otoacoustic emissions (DPOAE) measurements, and speed of auditory brain stem responses, which both until now were not thought to be controlled by TH, proved to be TH-dependent processes that were damaged by a delay of TH supply within this critical time. In contrast, no significant differences in the gross morphology and innervation of the organ of Corti or myelin gene expression in the auditory system, detected as myelin basic protein (MBP) and proteolipid protein (PLP) mRNA using Northern blot approach, were observed when TH supply was delayed for few days. These classical TH-dependent processes, however, were damaged when TH supply was delayed for several weeks. These surprising results may suggest the existence of different TH-dependent processes in the auditory system: those that respond to corrective TH supply (e.g., innervation and morphogenesis of the organ of Corti) and those that do not, but require T3 activity during a very tight time window (e.g., active cochlear process, central processes).

scholarly journals Thyroid hormones and fetal neurological development

2011 ◽  
Vol 209 (1) ◽  
pp. 1-8 ◽  
Author(s):  
J Patel ◽  
K Landers ◽  
H Li ◽  
R H Mortimer ◽  
K Richard
Keyword(s):  
Thyroid Hormone ◽  
Cell Membrane ◽  
Hormone Receptors ◽  
Developmental Stages ◽  
Fetal Brain ◽  
Neurological Development ◽  
Thyroid Hormone Metabolism ◽  
Pituitary Thyroid Axis ◽  
Fetal Thyroid ◽  
Type 3

The development of fetal thyroid function is dependent on the embryogenesis, differentiation, and maturation of the thyroid gland. This is coupled with evolution of the hypothalamic–pituitary–thyroid axis and thyroid hormone metabolism, resulting in the regulation of thyroid hormone action, production, and secretion. Throughout gestation there is a steady supply of maternal thyroxine (T4) which has been observed in embryonic circulation as early as 4 weeks post-implantation. This is essential for normal early fetal neurogenesis. Triiodothyronine concentrations remain very low during gestation due to metabolism via placental and fetal deiodinase type 3. T4 concentrations are highly regulated to maintain low concentrations, essential for protecting the fetus and reaching key neurological sites such as the cerebral cortex at specific developmental stages. There are many known cell membrane thyroid hormone transporters in fetal brain that play an essential role in regulating thyroid hormone concentrations in key structures. They also provide the route for intracellular thyroid hormone interaction with associated thyroid hormone receptors, which activate their action. There is a growing body of experimental evidence from rats and humans to suggest that even mild maternal hypothyroxinemia may lead to abnormalities in fetal neurological development. Our review will focus on the ontogeny of thyroid hormone in fetal development, with a focus on cell membrane transporters and TR action in the brain.

scholarly journals Chemokine Expression Is Involved in the Vascular Neogenesis of Ewing Sarcoma: A Preliminary Analysis of the Early Stages of Angiogenesis in a Xenograft Model

2018 ◽  
Vol 22 (1) ◽  
pp. 30-39
Author(s):  
Francisco Giner ◽  
José A López-Guerrero ◽  
Antonio Fernández-Serra ◽  
Isidro Machado ◽  
Empar Mayordomo-Aranda ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Tumor Cells ◽  
Nude Mice ◽  
Ewing Sarcoma ◽  
Xenograft Model ◽  
Bone Cancer ◽  
Mouse Serum ◽  
Early Stages ◽  
Peritumoral Stroma ◽  
Ligand Expression

Background Ewing sarcoma (EWS) is the second most common bone cancer in pediatric patients. Angiogenesis is a major factor for tumor growth and metastasis. Our aim was to carry out a histological, immunohistochemical, and molecular characterization of the neovascularization established between xenotransplanted tumors and the host during the initial phases of growth in nude mice in three angiogenesis experiments (ES2, ES3, and ES4). Methods The original human EWS were implanted subcutaneously on the backs of three nude mice. Tumor pieces 3 mm–4 mm in size from early passages of Nu432, Nu495, and Nu471 were also implanted subcutaneously on the backs of three sets (ES2, ES3, and ES4) of athymic Balb-c nude mice (n = 14 each). The animals were sacrificed at 24, 48, and 96 hours and at 7, 14, 21, and 28 days after implantation to perform histological, immunohistochemical, and molecular studies (neovascularization experiments). Results We observed histological, ultrastructural, and immunohistochemical changes in the xenografted tumor at different times after implantation. Chemokine ligand expression peaked twice, once during the first 48 hours and again in the second week. We observed that tumor cells in contact with murine peritumoral stroma presented higher expression of chemokine ligands as well as more tumor cells around the capillary vessels. Mouse serum vascular endothelial growth factor levels peaked twice, once in the first hours and then in the second week after tumor implantation. Conclusion Chemokines and other angiogenic factors may be relevant in the angiogenic mechanism during tumor growth. This model provides information on the early stages of the angiogenic process and could be a useful tool in researching anti-angiogenic drugs for new therapeutic strategies in EWS.

scholarly journals Maternal and placental responses before preterm birth: adaptations to increase fetal thyroid hormone availability?

2018 ◽  
Vol 32 (16) ◽  
pp. 2746-2757 ◽  
Author(s):  
An Eerdekens ◽  
Lies Langouche ◽  
Fabian Güiza ◽  
Johan Verhaeghe ◽  
Gunnar Naulaers ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Thyroid Hormone ◽  
Fetal Thyroid

scholarly journals Fetal Thyroid Hormone Level at Birth Is Associated with Fetal Growth

2011 ◽  
Vol 96 (6) ◽  
pp. E934-E938 ◽  
Author(s):  
Beverley M. Shields ◽  
Beatrice A. Knight ◽  
Anita Hill ◽  
Andrew T. Hattersley ◽  
Bijay Vaidya
Keyword(s):  
Birth Weight ◽  
Thyroid Hormone ◽  
Cord Blood ◽  
Thyroid Function ◽  
Fetal Growth ◽  
Late Gestation ◽  
Third Trimester ◽  
Free T4 ◽  
Skeletal Size ◽  
Fetal Thyroid

Context: Thyroid function is known to play an important role in fetal neurological development, but its role in regulating fetal growth is not well established. Overt maternal and fetal thyroid disorders are associated with reduced birth weight. We hypothesized that, even in the absence of overt thyroid dysfunction, maternal and fetal thyroid function influence fetal growth. Aim: In normal, healthy pregnancies, we aimed to assess whether fetal thyroid hormone at birth (as measured in cord blood) is associated with fetal growth. We also aimed to study whether fetal thyroid hormone at birth is associated with maternal thyroid hormone in the third trimester. Methods: In 616 healthy mother-child pairs, TSH, free T4 (FT4), and free T3 (FT3) were measured in mothers at 28 wk gestation and in umbilical cord blood at birth. Birth weight, length, head circumference, and tricep and bicep skinfold thicknesses were measured on the babies. Results: Cord FT4 was associated with birth weight (r = 0.25; P < 0.001), length (r = 0.17; P < 0.001), and sum of skinfolds (r = 0.19; P < 0.001). There were no associations between birth measurements and either cord TSH or cord FT3. Maternal FT4 and cord FT4 were correlated (r = 0.14; P = 0.0004), and there were weaker negative associations between maternal TSH and cord FT4 (r = −0.08; P = 0.04) and FT3 (r = −0.10; P = 0.01). Conclusion: Associations between cord FT4 and birth size suggest that fetal thyroid function may be important in regulating fetal growth, both of skeletal size and fat. The correlation between third-trimester maternal FT4 and cord FT4 supports the belief that maternal T4 crosses the placenta even in late gestation.

Characterization of rat iodothyronine sulfotransferases

2003 ◽  
Vol 285 (3) ◽  
pp. E592-E598 ◽  
Author(s):  
Monique H. A. Kester ◽  
Ellen Kaptein ◽  
Thirza J. Roest ◽  
Caren H. van Dijk ◽  
Dick Tibboel ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Rat Brain ◽  
Rat Liver ◽  
Rat Kidney ◽  
Female Rat ◽  
Reversible Inactivation ◽  
Fetal Thyroid ◽  
Important Pathway ◽  
Brain Cytosol

Sulfation appears to be an important pathway for the reversible inactivation of thyroid hormone during fetal development. The rat is an often used animal model to study the regulation of fetal thyroid hormone status. The present study was done to determine which sulfotransferases (SULTs) are important for iodothyronine sulfation in the rat, using radioactive T4, T3, rT3, and 3,3′-T2 as substrates, 3′-phosphoadenosine-5′-phosphosulfate (PAPS) as cofactor, and rat liver, kidney and brain cytosol, and recombinant rat SULT1A1, -1B1, -1C1, -1E1, -2A1, -2A2, and -2A3 as enzymes. Recombinant rat SULT1A1, -1E1, -2A1, -2A2, and -2A3 failed to catalyze iodothyronine sulfation. For all tissue SULTs and for rSULT1B1 and rSULT1C1, 3,3′-T2 was by far the preferred substrate. Apparent Km values for 3,3′-T2 amounted to 1.9 μM in male liver, 4.4 μM in female liver, 0.76 μM in male kidney, 0.23 μM in male brain, 7.7 μM for SULT1B1, and 0.62 μM for SULT1C1, whereas apparent Km values for PAPS showed less variation (2.0-6.9 μM). Sulfation of 3,3′-T2 was inhibited dose dependently by other iodothyronines, with similar structure-activity relationships for most enzymes except for the SULT activity in rat brain. The apparent Km values of 3,3′-T2 in liver cytosol were between those determined for SULT1B1 and -1C1, supporting the importance of these enzymes for the sulfation of iodothyronines in rat liver, with a greater contribution of SULT1C1 in male than in female rat liver. The results further suggest that rSULT1C1 also contributes to iodothyronine sulfation in rat kidney, whereas other, yet-unidentified forms appear more important for the sulfation of thyroid hormone in rat brain.

Effects of marginal iodine deficiency during pregnancy: iodide uptake by the maternal and fetal thyroid

1997 ◽  
Vol 273 (6) ◽  
pp. E1121-E1126 ◽  
Author(s):  
P. M. Versloot ◽  
J. P. Schröder-Van Der Elst ◽  
D. Van Der Heide ◽  
L. Boogerd
Keyword(s):  
Thyroid Hormone ◽  
Iodine Deficiency ◽  
Specific Activity ◽  
Hormone Production ◽  
Iodide Uptake ◽  
Deficient Diet ◽  
Pregnant Rats ◽  
Thyroid Hormone Metabolism ◽  
Fetal Thyroid ◽  
The Absolute

Iodide uptake by the thyroid is an active process. Iodine deficiency and pregnancy are known to influence thyroid hormone metabolism. The aim of this study was to clarify the effects of iodine deficiency and pregnancy on iodide uptake by the thyroid. Radioiodide was injected intravenously into nonpregnant and 19-day pregnant rats receiving a normal or marginally iodine-deficient diet. The uptake of radioiodide by the thyroid was measured continuously for 4 h. The absolute iodide uptake by the maternal and fetal thyroid glands at 24 h was calculated by means of the urinary specific activity. Pregnancy resulted in a decrease in the absolute thyroidal iodide uptake. Marginal iodine deficiency had no effect on the absolute iodide uptake by the maternal thyroid. The decreased plasma inorganic iodide was compensated by an increase in thyroidal clearance. A similar compensation was not found for the fetus; the uptake of iodide by the fetal thyroid decreased by 50% during marginal iodine deficiency. This can lead to diminished thyroid hormone production, which will have a negative effect on fetal development, especially of the brain.

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