• International journal of thyroidology
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• v.10 no.2
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• pp.71-76
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• 2017

Background and Objectives: The role of thyroid-stimulating hormone (TSH) signaling on osteoblastic differentiation is still undetermined. The aim of this study was to investigate the effects of 5-aza-2'-deoxycytidine (5-azacytidine) on TSH-mediated regulations of osteoblasts. Materials and Methods: MG63, a human osteoblastic cell-line, was treated with 5-azacytidine before inducing osteogenic differentiation using osteogenic medium (OM) containing L-ascorbic acid and ${\beta}$-glyceophosphate. Bovine TSH or monoclonal TSH receptor stimulating antibody (TSAb) was treated. Quantitative real-time PCR analyses or measurement of alkaline phosphatase activities were performed for evaluating osteoblastic differentiation. Results: Studies for osteogenic-related genes or alkaline phosphatase activity demonstrated that treatment of TSH or TSAb alone had no effects on osteoblastic differentiation in MG63 cells. However, treatment of 5-azacytidine, per se, significantly increased osteoblastic differentiation and combination treatment of 5-azacytidine and TSH or TSAb in the condition of OM showed further significant increase of osteoblastic differentiation. Conclusion: Stimulating TSH signaling has little effects on osteoblastic differentiation in vitro. However, in the condition of epigenetic modification using inhibitor of DNA methylation, TSH signaling positively affects osteoblastic differentiation in human osteoblasts.

• Biomedical Science Letters
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• v.14 no.1
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• pp.59-62
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• 2008

This experiment was performed to study the effect of TSH (thyroid-stimulating hormone) on the expression of endoplasmic reticulum (ER) chaperones in the rat thyrocytes FRTL-5 cells. Although the expressions of ER membrane kinases (ATF6, IRE1 and PERK) were specially enhanced under absence of TSH, no remarkable up- or down regulations of ER chaperones (BiP, CHOP and Calnexin) were detected by TSH. We firstly report here that TSH by dose up-regulated expression of ER membrane kinases in FRTL-5 culture thyrocytes.

• The Korean journal of sports medicine
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• v.36 no.4
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• pp.214-220
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• 2018

Purpose: The purpose of this research is to study changes in pituitary hormone in anterior lobe and thyroid hormone before, after, and during recovery time in severe 100 km ultramarathon. Methods: Healthy middle-aged runners (age, $52.0{\pm}4.8$ years) participated in the test. Grade exercise test is done, and then blood is taken from those participants before and after completing 100 km ultramarathon at the intervals of 24 hours (1 day), 72 hours (3 days), and 120 hours (5 days) to analyze their luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), and free thyroxine (Free T4). Results: For LH, it decreased more significantly at 100 km than pre-race. However, after 1 day result increased more than that of 100 km. At 3 days, it was significantly higher than pre-race and 100 km, recovering at 5 days. In terms of FSH, it decreased at 100 km, 1 day, and 3 days more than pre-race but recovered at 5 days. TSH was higher at 1 day and 5 days compared to pre-race. T3 was only higher at 100 km than pre-race. T4 was higher till 5 days at 100 km than pre-race. Free T4 increased more significantly at 100 km than pre-race. Conclusion: In terms of severe long distance running, LH and FSH which belong to hormone from anterior lobe as well as T3, T4, and Free T4 which belong to thyroid hormone showed their variation within the standard range. However, TSH showed abnormal increase from enhanced concentration of blood after marathon becoming hyper-activation even during the recovery period.

• Clinical and Experimental Pediatrics
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• v.50 no.6
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• pp.576-579
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• 2007

The syndrome of resistance to thyroid hormone (RTH) is characterized by reduced tissue sensitivity to thyroid hormone (TH). In the majority of subjects, RTH is caused by mutations in the thyroid hormone receptor beta ($TR{\beta}$) gene, located on the chromosome locus 3p24.3. RTH is inherited in an autosomal dominant manner. The clinical presentation of RTH is variable, but common features include elevated serum levels of thyroid hormone (TH), a normal or slightly increased thyrotropin (thyroid stimulating hormone, TSH) level that responds to thyrotropin releasing hormone (TRH), and goiter. We report a 4 year-old girl, who was clinically euthyroid in spite of high total and free $T_4$, and $T_3$ concentrations, while TSH was slightly increased. Sequence analysis of the thyroid hormone receptor beta gene (THRB) confirmed a heterozygous C to T change at nucleotide number 1303, resulting in a substitution of histidine by tyrosine at codon 435 (H435Y). Further analysis of her parents revealed that the H435Y variation was a de novo mutation since neither parents had the variation. Her parents' TH and TSH levels were within normal range.

• Journal of Korean Neurosurgical Society
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• v.63 no.4
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• pp.495-503
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• 2020

Objective : Thyroid-stimulating hormone (TSH)-secreting pituitary adenoma (PA) is an extremely rare functioning form of PA that accounts for 0.7-2% of all such cases. The previously reported outcomes of the surgical removal of TSH-PA are poor. Owing to its extremely low incidence, most available reports on TSH-PA are case reports or small case series. Thus, we investigated the clinical and endocrinological outcomes of surgically treated TSH-PA through our institutional series. Methods : We retrospectively reviewed 14 consecutive cases of surgically treated TSH-PA, focusing on the clinical, radiological, surgical, and endocrinological data. Results : There were seven male (50%) and seven female (50%) patients. The mean age was 42.5 years (range, 19-63). The mean tumor size was 16.6 mm (range, 4-30). Optic chiasm compression was noted in six patients (42.9%), and no patient showed cavernous sinus invasion. Thirteen of 14 patients (92.8%) underwent transnasal transsphenoidal approach (TSA), and one patient underwent TSA followed by transcranial approach for residual tumor removal. Thirteen of 14 patients (92.8%) showed endocrinological remission; all patients who experienced remission showed subnormal levels of TSH (<0.4 μU/mL) on postoperative day 2. Recurrence occurred in two patients (14.2%). One patient underwent subsequent revision transnasal TSA for recurrent tumor removal, and the other patient underwent gamma knife radiosurgery for recurrence. Conclusion : Surgical treatment showed excellent surgical outcomes. The TSH level in the immediate postoperative period may be a predictor for endocrinological remission.

• Journal of Chest Surgery
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• v.26 no.10
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• pp.743-748
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• 1993

Alterations in thyroid function test results are frequently seen in patients with nonthyroidal illness & correlate with the severity of the illness & prognosis. We studied thyroid hormone changes in 14 patients received cardiopulmonary bypass[CPB]. All patients were biochemical euthyroidism preoperatively. TSH[Thyroid Stimulating Hormone] level reached its nadir[0.46 $\pm$ 0.11 ulU/ml, P<0.0005] at 12 hours after the start of CPB & showed elevating pattern to the preoperative level thereafter. FT4[Free Thyroxine] reached to its nadir[10.16$\pm$ 1.17 pmol/L, P<0.01] at POD[Post Operative Day] #4 & reached to the preoperative level at POD #7. Mean serum TSH & FT4 concentration were within normal limits[P>0.25] during CPB & thereafter. TT3[Total Triiodothyronine] reached to its nadir[38.6 $\pm$ 8.4 ng/dl, P<0.001] at 30 minutes after the start of CPB & remained low[P<0.05] throughout the study period. The patients whose recovery was uneventful[Group I] had higher serum TSH, TT3 levels[P<0.05] than who had complications or died[Group II]. Group I showed the elevating pattern of TSH, TT3 at POD #4, but Group II failed to show such elevating pattern. In Group I, FT4 was within normal limits[P>0.5] throughout the study period, and also within normal limits[P>0.1] in Group II.

• Animal cells and systems
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• v.6 no.3
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• pp.239-245
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• 2002

Plasma melatonin, thyroid-stimulating hormone (TSH) and body temperature were measured simultaneously and continuously before and after the sleep-wake cycle was shifted in 4 healthy males and changes in the circadian rhythm itself and in the phase relationship among these circadian rhythms were determined. Normal sleep-wake cycle (sleep hours: 2300-0700) was delayed by 10 h (sleep hours: 0900-1700) during the experiment. Even after this shift the typical melatonin rhythm was maintained: low during daytime and high during night. The melatonin rhythm was gradually delayed day by day. The TSH rhythm was also maintained fundamentally during 3 consecutive days of altered sleep-wake cycle. The phase was also delayed gradually but remarkably. The daily rhythm of body temperature was changed by the alteration of sleep-wake cycle. The body temperature began to decrease at the similar clock time as in the control but the decline during night awake period was less steep and the lowered body temperature persisted during sleep. The hormonal profiles during the days of shifted sleep/wake cycle suggest that plasma melatonin and TSH rhythms are basically regulated by an endogenous biological clock. The parallel phase shift of melatonin and TSH upon the change in sleep-wake cycle suggests that a common unitary pacemaker probably regulates these two rhythms. The reversal phase relationship between body temperature and melatonin suggests that melatonin may have a hypothermic effect on body temperature. The altered body temperature rhythm suggests that the awake status during night may inhibit the circadian decrease in body temperature and that sleep sustains the lowered body temperature. It is probable but uncertain that there ave causal relationships among sleep, melatonin, TSH, and body temperature.

• Clinical and Experimental Pediatrics
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• v.62 no.3
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• pp.85-89
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• 2019

Purpose: We compared thyroid hormone profiles in children with nephrotic syndrome (NS) during the nephrotic phase and after remission. Methods: This study included 31 pediatric NS patients. The thyroid hormone profiles included serum levels of triiodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH), and free T4. Results: Of the 31 patients, 16 (51.6%) showed abnormal thyroid hormone profiles: 6 had overt hypothyroidism, 8 had subclinical hypothyroidism, and 2 had low T3 syndrome. The mean serum T3, T4, and free T4 levels in the nephrotic phase and after remission were $82.37{\pm}23.64$ and $117.88{\pm}29.49ng/dL$, $5.47{\pm}1.14$ and $7.91{\pm}1.56{\mu}g/dL$, and $1.02{\pm}0.26$ and $1.38{\pm}0.23ng/dL$, respectively; the levels were significantly lower in the NS nephrotic phase (P=0.0007, P<0.0001, and P=0.0002). The mean serum TSH levels during the nephrotic phase and after remission were $8.05{\pm}3.53$ and $4.08{\pm}2.05{\mu}IU/mL$, respectively; they were significantly higher in the nephrotic phase (P=0.0005). The urinary protein/creatinine ratio during the nephrotic phase was significantly correlated with serum T3, T4, and free T4 levels (r=-0.5995, P=0.0032; r=-0.5797, P=0.0047; r=-0.5513, P=0.0078) as well as with TSH levels (r=0.5022, P=0.0172). A significant correlation was found between serum albumin and serum T3 levels during the nephrotic phase (r=0.5385, P=0.0018) but not between serum albumin and T4, TSH, or free T4 levels. These significant correlations all disappeared after remission. Conclusion: Abnormal thyroid hormone profile findings were observed in 51.6% of pediatric patients with NS. Thyroid hormone levels normalized after remission, regardless of levothyroxine therapy.

• Clinical and Experimental Pediatrics
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• v.58 no.6
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• pp.224-229
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• 2015

Purpose: Thyroid dysfunction is common in preterm infants. Congenital hypothyroidism causes neurodevelopmental impairment, which is preventable if properly treated. This study was conducted to describe the characteristics of thyroid dysfunction in very low birth weight infants (VLBWIs), evaluate risk factors of hypothyroidism, and suggest the reassessment of thyroid function with an initially normal thyroid-stimulating hormone (TSH) as part of a newborn screening test. Methods: VLBWIs (January 2010 to December 2012) were divided into two groups according to dysfunction-specific thyroid hormone replacement therapy, and associated factors were evaluated. Results: Of VLBWIs, 246 survivors were enrolled. Only 12.2% (30/246) of enrolled subjects exhibited thyroid dysfunction requiring thyroid hormone replacement. Moreover, only one out of 30 subjects who required thyroid hormone treatment had abnormal thyroid function in the newborn screening test with measured TSH. Most of the subjects in the treatment group (22/30) exhibited delayed TSH elevation. Gestational age, Apgar score, antenatal steroids therapy, respiratory distress syndrome, patent ductus arteriosus, sepsis, intraventricular hemorrhage, postnatal steroids therapy, and duration of mechanical ventilation did not differ between the two groups. Birth weight was smaller and infants with small for gestational age were more frequent in the treatment group. Conclusion: Physicians should not rule out suggested hypothyroidism, even when thyroid function of a newborn screening test is normal. We suggest retesting TSH and free thyroxine in high risk preterm infants with an initially normal TSH level using a newborn screening test.

• Journal of Interdisciplinary Genomics
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• v.5 no.2
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• pp.32-34
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• 2023

Resistance to thyroid hormone syndrome (RTH) is a genetic disease caused by the mutation of either the thyroid hormone receptor-β (THRB) gene or the thyroid hormone receptor-α (THRA) gene. RTH caused by THRB mutations (RTH-β) is characterized by the target tissue's response to thyroid hormone, high levels of triiodothyronine and/or thyroxine, and inappropriate secretion of thyroid-stimulating hormone (TSH). THRA mutation is characterized by hypothyroidism that affects gastrointestinal, neurological, skeletal, and myocardial functions. Most patients do not require treatment, and some patients may benefit from medication therapy. These syndromes are characterized by decreased tissue sensitivity to thyroid hormones, generating various clinical manifestations. Thus, clinical changes of resistance to thyroid hormones must be recognized and differentiated, and an approach to the practice of personalized medicine through an interdisciplinary approach is needed.