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1 total and free thyroxine, and total and free triiodothyronine.
2 5'-deiodination of thyroxine to form 3,5,3'-triiodothyronine.
3 roxine (T4) to its active metabolite, 3,5,3'-triiodothyronine.
4 ferase activity by about 90% with or without triiodothyronine.
5 alamus was diminished by coadministration of triiodothyronine.
6 and T4 were suppressed by administration of triiodothyronine.
8 cultured human epidermal keratinocytes, with triiodothyronine (100 pmol/L) or thyroxine (100 nmol/L).
9 was induced by daily injection of l-3,5, 3'-triiodothyronine (15 ug (100 g)-1) intraperitoneally dai
10 6-dihydroxyindole-2-carboxylic acid, 3,3',5'-triiodothyronine, 3,3',5-triiodothyronine, gentisate, ro
11 ddition, we evaluated the in vitro effect of triiodothyronine, 9-cis-retinoic acid, and the retinoid
13 ent with either 10 nM dexamethasone or 10 nM triiodothyronine accelerated SC development and barrier
14 ing concentrations of leptin, thyroxine, and triiodothyronine act coordinately to favor weight regain
17 hyronine among women and with total and free triiodothyronine among men in lipid-standardized models.
18 h greater total and free thyroxine and total triiodothyronine among women and with total and free tri
20 orter function is reflected in elevated free triiodothyronine and lowered free thyroxine levels in th
21 terventions described were desmopressin use, triiodothyronine and methylprednisolone replacement, flu
25 ormation of (131)I-labeled levothyroxine and triiodothyronine and thereby reduce the protein-bound (1
26 treatment significantly increased uptake of triiodothyronine and thyroxine (4.1- and 4.3-fold, respe
28 icantly higher circulating concentrations of triiodothyronine and thyroxine at the end of the VLED th
29 could be attributed to decreased circulating triiodothyronine and thyroxine concentrations secondary
30 ssential constituent of the thyroid hormones triiodothyronine and thyroxine, which are required for t
31 differentiation method supplemented with T3 (triiodothyronine) and/or Dex (dexamethasone) during days
32 verts thyroxine to the active hormone 3,5,3'-triiodothyronine, and in the rat is expressed in the bra
33 analysis, changes in skeletal muscle, plasma triiodothyronine, and kidney masses explained 34.9%, 5.3
34 crease in serum levels of thyroxine, reverse triiodothyronine, and thyroid-stimulating hormone and a
35 els of total thyroxine, free thyroxine, free triiodothyronine, and thyroid-stimulating hormone were m
37 cal levels of active thyroid hormone (3,3',5-triiodothyronine) are controlled by the action of activa
38 ropin and the thyroid hormones thyroxine and triiodothyronine) are sometimes used as indicators of io
39 those for the thyroid hormones thyroxine and triiodothyronine, are among the clinical procedures for
43 id produced a more rapid rise in total serum triiodothyronine concentration and a higher total peak s
45 concentration and a higher total peak serum triiodothyronine concentration than the other products,
48 the extract of the coactivator function in a triiodothyronine-dependent manner and markedly impaired
49 second included four studies and showed that triiodothyronine did not add hemodynamic benefits versus
52 -stimulating hormone, total thyroxine, total triiodothyronine, free thyroxine, free triiodothyronine,
53 eptin significantly increased levels of free triiodothyronine, free thyroxine, insulin-like growth fa
56 RL), thyroid stimulating hormone (TSH), free triiodothyronine (fT3), and free thyroxin (fT4) were mea
58 nergy expenditure, percentage body fat, free triiodothyronine (FT3), urinary norepinephrine, and plas
59 xylic acid, 3,3',5'-triiodothyronine, 3,3',5-triiodothyronine, gentisate, rosmarinate, and 3-nitrotyr
62 nuclear in both the absence and presence of triiodothyronine; however, triiodothyronine induced a nu
63 hydrocortisone + placebo group 167 +/- 286; triiodothyronine + hydrocortisone group 466 +/- 495; p =
66 1 nm) were >100-fold more potent than 3,5,3'-triiodothyronine in initiating vesicle binding to actin
67 id inactivation of circulating thyroxine and triiodothyronine in patients with hemangiomas and its bl
69 weight loss, whereas serum concentrations of triiodothyronine increased significantly (by approximate
72 e and presence of triiodothyronine; however, triiodothyronine induced a nuclear reorganization of TRb
73 nd fasting blood biochemistry indexes (total triiodothyronine, insulin, leptin, and ghrelin) as indep
75 thyroxin to the biologically active 3,5, 3'-triiodothyronine, is highly concentrated in a group of s
76 is needed to allow for steady delivery of L-triiodothyronine" (it currently reads "... for steady de
78 es for muscimol in the presence of 3,3', 5-L-triiodothyronine (L-T3) indicated a noncompetitive inhib
79 erefore examined the effects of TH (L-3,3',5-triiodothyronine, L-T3) given to TH-deprived and to inta
82 here were also no differences in circulating triiodothyronine levels between groups at the end of the
87 e prohormone thyroxine to the active hormone triiodothyronine, modifying the expression of approximat
91 there is a perception that adding synthetic triiodothyronine, or liothyronine, to levothyroxine impr
92 total triiodothyronine, free thyroxine, free triiodothyronine, parathyroid hormone, prolactin, N-term
93 mug/kg; placebo + placebo group 208 +/- 392; triiodothyronine + placebo group 501 +/- 370; hydrocorti
94 hour IV infusion of 1) placebo + placebo, 2) triiodothyronine + placebo, 3) hydrocortisone + placebo,
96 ue reveals a novel mechanism for controlling triiodothyronine production that provides the first exam
98 igation and puncture, with or without 3,5,3'-triiodothyronine replacement (3 ng/hr), or sham surgery.
99 hyroid-stimulating hormone (TSH), thyroxine, triiodothyronine resin uptake, and free thyroxine index
100 In previous work, we characterized a 3,5,3'-triiodothyronine response element (T3RE) in acetyl-CoA c
101 siently transfected with plasmids containing triiodothyronine response elements and a minimal promote
102 ganded TR.RXR recruits both complexes to the triiodothyronine-responsive region of growth hormone gen
103 isoform is mainly limited to the pituitary, triiodothyronine-responsive TRH neurons, the developing
104 circulating concentrations of thyroxine and triiodothyronine returned to pre-weight-loss levels.
105 ence or absence of cycloheximide or 3,3', 5'-triiodothyronine (reverse T3, rT3) in rat pituitary tumo
106 values of 75-100 microM included 3,3', 5'-l-triiodothyronine (reverse T3; r-T3), 3,3'-diiodo-L-thyro
107 ta: L-triiodothyronine, TH, TH receptor, and triiodothyronine (reverse) were inferred as upstream reg
108 id hormones, including 3,3'-diiodothyronine, triiodothyronine, reverse triiodothyronine, and thyroxin
109 was derived from the T4 metabolite, reverse triiodothyronine (revT3), while functional studies provi
110 to 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) by the outer- and inner-ring deio
111 increase in rat HCN2 mRNA is likely due to L-triiodothyronine stimulation of HCN2 gene transcription.
112 ee thyroxine, but not the minimal isoform of triiodothyronine, suggesting that chronic anti-VEGF trea
116 f acute illness, namely a decrease in 3,5,3'-triiodothyronine (T(3)) and thyroid-stimulating hormone
117 compared the effectiveness of lithium versus triiodothyronine (T(3)) augmentation as a third-step tre
119 The thyroid hormones thyroxine (T(4)) and triiodothyronine (T(3)) play key roles in regulating dev
120 n between SREBP-1c, nuclear factor Y, 3,5,3'-triiodothyronine (T(3)) receptors, and co-activators usi
123 expression of target genes in the absence of triiodothyronine (T(3)) through the recruitment of the c
126 T(4) is enzymatically deiodinated to 3,5,3'-triiodothyronine (T(3)), a high-affinity ligand for the
127 g hormone (TSH), free thyroxine (T(4)), free triiodothyronine (T(3)), and leptin concentrations were
129 nown, highly potent physiological TR ligand, triiodothyronine (T(3)), and with a synthetic TR antagon
130 effects of administering a primary mitogen, triiodothyronine (T(3)), at the time of 70% partial hepa
133 ear receptors (TRs alpha and beta) that bind triiodothyronine (T(3), 3,5,3'-triiodo-l-thyronine) with
134 n whom T(4) replacement was stopped (without triiodothyronine [T(3)] replacement) in preparation for
135 we evaluated the ability of thyroid hormone (triiodothyronine [T(3)]), a known hepatic mitogen, to st
138 pe 2 deiodinase (D2), which generates 3,5,3'-triiodothyronine (T3 ), the active thyroid hormone.
139 (10 mU ml(-1)), thyroxine (T4) (100 nM), and triiodothyronine (T3) (100 pM) alter intrafollicular mit
140 Ralpha and TRbeta plays an important role in triiodothyronine (T3) action and TR isoform specificity.
142 e the conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3)
143 erapy results in relatively low serum 3,5,3'-triiodothyronine (T3) and high serum thyroxine/T3 (T4/T3
145 and cardiac abnormalities were alleviated by triiodothyronine (T3) and T4 administration to pups, by
147 on the effects of Hg on the thyroid hormones triiodothyronine (T3) and thyroxine (T4) in aquatic wild
148 congeners, total and free thyroid hormones (triiodothyronine (T3) and thyroxine (T4)), thyroid-stimu
149 levels were associated with lower cord total triiodothyronine (T3) and total T4 levels, and maternal
150 evels of thyroid hormones thyroxine (T4) and triiodothyronine (T3) averaged 46.9 and 64%, respectivel
151 ecruitment in vitro, while preserving normal triiodothyronine (T3) binding and CoR interactions.
155 ly in life, D3KO mice exhibit delayed 3,5,3'-triiodothyronine (T3) clearance, a markedly elevated ser
156 e report that despite a normal plasma 3,5,3'-triiodothyronine (T3) concentration, cold-exposed mice w
157 ate of adrenergic overactivity prevails when triiodothyronine (T3) concentrations become excessive, t
158 changes in gene expression and plasma 3,3',5-triiodothyronine (T3) concentrations in tadpoles treated
159 nd ligand-binding protein to decrease T4 and triiodothyronine (T3) cross-reactivity with the antibody
160 eir wild-type counterparts were treated with triiodothyronine (T3) for 14 days and compared to untrea
161 e of a critical role for the thyroid hormone triiodothyronine (T3) in controlling the maturation and
163 sor thyroxine (T4) to the active form 3,5,3'-triiodothyronine (T3) in the blood is many times higher
164 Treatment of endothelial cells with L-3,5,3'-triiodothyronine (T3) increased the association of TRalp
165 ed to determine if fetal plasma cortisol and triiodothyronine (T3) influenced the mRNA abundance of U
174 a (ACCalpha) promoter 2 that mediated 3,5,3'-triiodothyronine (T3) regulation of ACCalpha transcripti
175 on of the human N-Tera-2 (NT2) cell line, in triiodothyronine (T3) replete and T3-depleted media.
179 roteins decreased by 50%, and treatment with triiodothyronine (T3) restored ubiquitination to control
180 Addition of the thyroid hormone 3,5,3'-L-triiodothyronine (T3) resulted in reversal of this repre
183 yroxine (T4) and supplies most of the 3,5,3'-triiodothyronine (T3) that is essential for brain develo
185 nase thought to provide intracellular 3,5,3' triiodothyronine (T3) to a restricted group of tissues.
186 efined sleep of acute restoration of l-3,3'5-triiodothyronine (T3) to a sleep-regulatory brain region
187 rk has shown that acute microinjections of l-triiodothyronine (T3) to the preoptic region significant
188 er cone loss) were used to determine whether triiodothyronine (T3) treatment (stimulating TH signalin
189 me (NTIS), characterized by low serum 3,5,3'-triiodothyronine (T3) with normal l-thyroxine (T4) level
190 range and levels of free thyroxine (FT4) and triiodothyronine (T3) within the reference range are com
191 hyroid histology, plasma thyroxine (T4), and triiodothyronine (T3), and hepatic outer ring deiodinati
193 to the metabolically active molecule 3,5,3'-triiodothyronine (T3), but its global inactivation unexp
194 hed when the normal prepartum rise in plasma triiodothyronine (T3), but not cortisol, was prevented b
195 BDEs were not strongly associated with total triiodothyronine (T3), free T4, or thyroid-stimulating h
196 condition, antibody response to vaccination, triiodothyronine (T3), hepatic biotransformation (7-etho
197 nstrate a negative role of one such hormone, triiodothyronine (T3), in triggering the differentiation
200 issues convert the prohormone thyroxine into triiodothyronine (T3), the active ligand for the thyroid
201 (D2) that activates thyroxine (T4) to 3,3',5-triiodothyronine (T3), the disruption of which (Dio2(-/-
203 serum thyrotropin-stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), and free T4 conce
205 ulin), which contain both thyroxine (T4) and triiodothyronine (T3), were the first pharmacologic trea
208 (as studied in several laboratories), and by triiodothyronine (T3), which has not been previously exa
209 ter-transcription factor (COUP-TF) represses triiodothyronine (T3)-dependent transcriptional activati
210 ted dominant negative activity as it blocked triiodothyronine (T3)-mediated transcriptional activity
211 assays showed that TRalpha failed to support triiodothyronine (T3)-stimulated transcription on "inact
222 ial organ donor can include thyroid hormone (triiodothyronine [T3] or levothyroxine [T4]), corticoste
223 yme that inactivates thyroid hormone (3,5,3' triiodothyronine [T3]), is frequently expressed by tumor
224 ter is responsive to thyroid hormone (3,3',5-triiodothyronine, T3) and efficiently repressed by unlig
225 dels with a hyperthyroid-like phenotype, TH (triiodothyronine, T3), in culture and exercise in vivo.
226 localized regulation of levels of active TH (triiodothyronine, T3), through spatiotemporal expression
231 and functions were inferred from the data: L-triiodothyronine, TH, TH receptor, and triiodothyronine
232 ned more non-thyroglobulin-associated T4 and triiodothyronine than did those in wild-type mice, indep
233 ne, which undergoes peripheral conversion to triiodothyronine, the active form of thyroid hormone.
234 wing ligands: deoxycholate, 5-leuenkephalin, triiodothyronine, thyronine, dabsyl-L-valine, and N-benz
236 genous and xenobiotic compounds, including L-triiodothyronine, thyroxine, estrone, p-nitrophenol, 2-n
237 on is achieved through the binding of 3,5,3'-triiodothyronine to its nuclear receptor, which results
238 paper, we demonstrate that binding of TH T3 (triiodothyronine) to THRB induces senescence and deoxyri
241 circulating total thyroxine (TT4) and 3,5,3'-triiodothyronine (TT3), respectively, while TT4 and TT3
242 free thyroxine [TT4 and FT4], total and free triiodothyronine [TT3 and FT3], thyroid-stimulating horm
243 hy men treated for 14 days with 75 microg of triiodothyronine, using 24,000 cDNA element microarrays.
245 ty acid synthase gene by the thyroid hormone triiodothyronine, various constructs of the human fatty
246 accelerating the conversion of thyroxine to triiodothyronine via type 2 deiodinase in mouse skeletal
247 No change in levels of serum thyrotropin or triiodothyronine was detected, although the thyroxine le
248 rast, the decline of TSH by treatment with L-triiodothyronine was severely blunted in SRC-1(-/-) mice
251 ine excretion and in serum concentrations of triiodothyronine were significantly correlated with perc
252 r binding activities, putative receptors for triiodothyronine, were detected after incubation of horm
253 and propionic acid analogs of thyroxine and triiodothyronine, which are inseparable by currently ava
254 id, the prohormone thyroxine is converted to triiodothyronine, which is essential in brain developmen
255 lysates activate thyroxine (T(4)) to 3,5,3'-triiodothyronine with typical characteristics of D2 such
256 ine the safety and efficacy of administering triiodothyronine, with and without hydrocortisone, in a
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