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1 infant thyroid-stimulating hormone and free thyroxine.
2 mide derivatives of thyroxine or deiodinated thyroxine.
3 ormation of impurities in thermally stressed thyroxine.
4 ring the biosynthesis of the thyroid hormone thyroxine.
5 ssociated with both free thyroxine and total thyroxine.
6 total antioxidant power was not affected by thyroxine.
7 the two binding sites for the natural ligand thyroxine.
8 y measurements of serum thyrotropin and free thyroxine.
9 vasopressin and either triiodothyronine or L-thyroxine.
10 vasopressin and either triiodothyronine or l-thyroxine.
11 ve became hypothyroid and required long-term thyroxine.
12 ocesses could be inhibited by probucol and L-thyroxine.
14 ne, tetramethylrosamine, fluoride, dopamine, thyroxine, 2,4-dinitrotoluene) and activated gene expres
16 tly increased uptake of triiodothyronine and thyroxine (4.1- and 4.3-fold, respectively), which was a
17 much longer half-life of D3 (12 h) than the thyroxine activating members of the selenodeiodinase fam
18 ated reduction of the type 2 deiodinase, the thyroxine-activating enzyme, and both effects are revers
19 s alone and steroids plus triiodothyronine/l-thyroxine also significantly reduced prolonged graft dys
20 mong these women, associations between total thyroxine and concurrent 1996 TCDD were slightly weaker
21 h hyperthyroidism are low TSH, elevated free-thyroxine and free-triiodothyronine levels, and TSH-rece
24 vidence that transthyretin, a transporter of thyroxine and retinol, is aggregated in preeclampsia and
25 nvolved in the transportation of the hormone thyroxine and retinol-binding protein, in the myocardium
27 , one of which defines the binding sites for thyroxine and small-molecule amyloidogenesis inhibitors.
29 rameric protein involved in the transport of thyroxine and the vitamin A-retinol-binding protein comp
32 antly associated with greater total and free thyroxine and total triiodothyronine among women and wit
33 pacity for rapid inactivation of circulating thyroxine and triiodothyronine in patients with hemangio
34 stem tone, and circulating concentrations of thyroxine and triiodothyronine returned to pre-weight-lo
35 hormone thyrotropin and the thyroid hormones thyroxine and triiodothyronine) are sometimes used as in
36 on, including those for the thyroid hormones thyroxine and triiodothyronine, are among the clinical p
38 TSH (thyroid-stimulating hormone), FT4 (free thyroxine) and gait, without known thyroid disease or de
39 ) for statins, 1.40 (95% CI: 1.02, 1.92) for thyroxine, and 1.53 (95% CI: 1.04, 2.24) for insulin.
41 s well as thyroid-stimulating hormone, total thyroxine, and free thyroxine, were measured in serum sa
42 centrations of plasma tri-iodothyronine, low thyroxine, and normal range or slightly decreased concen
43 10 case-control pairs were assessed for free thyroxine, and sera of 948 case-control pairs were asses
45 ne and circulating concentrations of leptin, thyroxine, and triiodothyronine act coordinately to favo
49 that the TTR amyloid is incapable of binding thyroxine as monitored by either isothermal calorimetry
50 e stable isotopic thyroid hormone (13)C(6)-L-thyroxine as the label of which the binding to rTTR is i
51 s, resulting in the formation of deiodinated thyroxines, as well as acetic acid, benzoic acid, formal
52 in (Tg) T cell epitope p2549-2560 containing thyroxine at position 2553 (T4p2553) induces thyroiditis
53 ted six promoters, CMV, EF1alpha, PGK, apoE, thyroxine binding globulin (TBG), and cytochrome P450 2E
57 tion in vitro via an interaction between the thyroxine binding pocket of the TTR tetramer and Abeta r
59 t only utilizes the outer portion of the two thyroxine binding pockets to bind to and inhibit TTR amy
60 he homotetrameric TTR contains two identical thyroxine binding pockets, occupation of which by specif
62 units whose quaternary interface defines the thyroxine binding site also dramatically increases the b
63 Binding of small molecule ligands within the thyroxine binding site of TTR can stabilize the tetramer
64 ivity enables these inhibitors to occupy the thyroxine binding site(s) in a complex biological fluid
69 Although revealing the ability of the two thyroxine binding sites of TTR to discriminate between d
70 tion state by small molecule binding to both thyroxine binding sites raises the kinetic barrier of te
72 yl known to have high affinity for the inner thyroxine binding subsite of transthyretin (TTR) was con
73 injecting adeno-associated virus containing thyroxine-binding globulin promoter-driven causes recomb
74 were injected with adeno-associated virus 8-thyroxine-binding globulin-Cre-recombinase versus contro
75 and ~200 nM) to the two normally unoccupied thyroxine-binding sites of the tetramer, and kinetically
77 ghly preferential binding of resveratrol and thyroxine, both characterized by negative binding cooper
78 the relationship between 1976 TCDD and total thyroxine but drove the association with 1996 TCDD to th
79 evel of the predominant thyroid hormone free thyroxine, but not the minimal isoform of triiodothyroni
81 xinemia, characterized by low levels of free thyroxine coexisting with reference thyrotropin levels,
83 o decreased circulating triiodothyronine and thyroxine concentrations secondary to reduced mRNA expre
87 18-30 microM included L-thyroxine (L-T4), D-thyroxine (D-T4), 3,3', 5,5'-tetraiodothyroacetic acid (
88 lpha), collagen I and III transcription, and thyroxine decreased cyclin-dependent kinase inhibitor 2A
89 ipation, which improved after treatment with thyroxine, despite normal concentrations of circulating
90 h SCH and high symptom burden at baseline, L-thyroxine did not improve hypothyroid symptoms or tiredn
92 ough it is reasonable to expect a need for a thyroxine dose increase with some antiepileptic drugs, t
93 A continuous infusion of 4 mug/kg per day thyroxine for 42 days can safely correct transient hypot
94 injected either with growth hormone (GH) or thyroxine for a 6-wk period to see whether this interven
96 981) and 1996 (n = 260), and levels of total thyroxine, free thyroxine, free triiodothyronine, and th
97 = 260), and levels of total thyroxine, free thyroxine, free triiodothyronine, and thyroid-stimulatin
98 otal thyroxine, total triiodothyronine, free thyroxine, free triiodothyronine, parathyroid hormone, p
99 peech), biochemical (subnormal ratio of free thyroxine:free tri-iodothyronine [T3], low concentration
100 ethylhexyldiphenyl phosphate (EHDP) and free thyroxine (FT(4)), between BDE-100 and free triiodothyro
102 0.70; 95% CI: -1.06, -0.34], decreasing free thyroxine (fT4) (beta = -0.053; 95% CI: -0.092, -0.013),
103 ne, or TSH) level with normal levels of free thyroxine (FT4) affects up to 10% of the adult populatio
104 cted thyroid stimulating hormone (TSH), free thyroxine (FT4) and thyroid peroxidase antibody (TPOAb)
105 and where free triiodothyronine (fT3), free thyroxine (fT4) and thyroid stimulating hormone (TSH) wa
106 tside the reference range and levels of free thyroxine (FT4) and triiodothyronine (T3) within the ref
107 H using Cox regression and outcomes and free thyroxine (FT4) concentration using restricted cubic-spl
108 l thyroid-stimulating hormone (TSH) and free thyroxine (fT4) levels with plasma concentrations of six
110 ars with thyroid-stimulating hormone or free thyroxine (FT4) measurements and clinical follow-up were
111 s of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and thyroglobulin, vary widely due to v
112 oncentrations of triiodothyronine (T3), free thyroxine (FT4), thyroid peroxidase antibody (Anti-TPO),
114 le thyroid traits thyrotropin (TSH) and free thyroxine (FT4), we analyse whole-genome sequence data f
115 TCEP had additional overall effects on free thyroxine (FT4), whereas TDCIPP also influenced total th
117 id-stimulating hormone (TSH), free and total thyroxine (fT4, TT4) and triiodothyronine (fT3, TT3), an
118 unction tests (serum thyrotropin [TSH], free thyroxine [fT4], and thyroid peroxidase [TPO] antibodies
119 by solid phase synthesis with immobilised L-thyroxine, glucosamine, fumonisin B2 or biotin as templa
120 ithin the ER with no detectable synthesis of thyroxine, had persistent exposure of free cysteine thio
122 growth factor, insulin-like growth factor-1, thyroxine, hepatocyte growth factor, and bone morphogene
124 Replacement treatment exists in the form of thyroxine, hydrocortisone, sex steroids, growth hormone,
126 ransthyretin is a transporter of retinol and thyroxine in blood, cerebrospinal fluid, and the eye, an
127 tly shown to reduce levels of free and total thyroxine in experimental animal studies, the direction
128 antiepileptic drugs, the effect of excessive thyroxine in lowering seizure threshold should also be c
129 converting enzyme (ACE), and measuring serum thyroxine in mice given anti-TGFbeta1 or the ACE inhibit
131 e was derived for the thermal degradation of thyroxine in the solid state, using data obtained from u
132 ses for 3 medications (statins, insulin, and thyroxine) in relation to 3 outcomes (retinal detachment
134 ine, triiodothyronine resin uptake, and free thyroxine index (FTI), were determined before initiation
135 The concentration of thyroxine and the free thyroxine index were higher in the ISP56 group, and the
139 reased levels of free triiodothyronine, free thyroxine, insulin-like growth factor 1, insulin-like gr
140 Originating in the thyroid, the prohormone thyroxine is converted to triiodothyronine, which is ess
143 ith IC(50) values of 18-30 microM included L-thyroxine (L-T4), D-thyroxine (D-T4), 3,3', 5,5'-tetraio
144 triiodothyronine was detected, although the thyroxine level decreased in patients receiving eprotiro
149 ontrols, the knock-outs had markedly reduced thyroxine levels ( approximately 50-80%) and profoundly
150 ncreased in a linear manner with higher free thyroxine levels (hazard ratio, 2.41; confidence interva
153 outside the reference range with normal free thyroxine levels in asymptomatic patients, is associated
161 inished weight gain and reduced plasma total thyroxine levels were found in both groups compared with
163 prid increased in the spleen, fawn survival, thyroxine levels, jawbone lengths, body weight, and orga
169 improved similarly between those receiving L-thyroxine (mean within-group change, -12.3 [95% CI, -16.
170 were also similar between those receiving L-thyroxine (mean within-group change, -8.9 [CI, -14.5 to
171 bulin (mean: +20.1%; 95% CI: 9.0, 32.2%) and thyroxine (mean: +1.5%; 95% CI: 0.0, 3.0%) increased per
173 uggests mechanisms for the inadequacies of l-thyroxine monotherapy and highlights the possible role f
175 The last sentence of the section titled "L-Thyroxine Monotherapy Fails to Restore All Markers of Hy
176 has brought into question the inability of l-thyroxine monotherapy to universally normalize serum T3
177 on provided a physiologic means to justify l-thyroxine monotherapy, obviating concerns about inconsis
181 tabilizer of TTR in vitro that occupies both thyroxine pockets and the intramolecular channel between
182 significant competition for resveratrol and thyroxine preferential binding sites and lacked the abil
183 ons of polyphenols with both resveratrol and thyroxine preferential binding sites, by using resveratr
185 variate analysis, age, treatment group, free thyroxine, protein, and magnesium levels were associated
187 idism that must be treated with aggressive L-thyroxine replacement and other supportive measures in t
190 d the selection of conditions for removal of thyroxine's free fraction from samples without significa
193 ypothyroidism was defined by an above normal thyroxine-stimulating hormone concentration or by the ne
194 products" like the synthetic thyroid hormone thyroxine, strict regulations enforce a detailed chemica
195 he applied therapy, combined with adequate L-thyroxine substitution, as well as vitamin D and seleniu
197 ized interaction between the thyroid hormone thyroxine (T(4)) and the proinflammatory cytokine macrop
198 on of the contrast agent were collected, and thyroxine (T(4)) and thyroid-stimulating hormone (TSH) l
200 emical thyroidectomy on the one hand, and by thyroxine (T(4)) and triiodothyronine (T(3)) replacement
201 ear thyroid hormone receptor TRbeta1 (TR), L-thyroxine (T(4)) causes activation and nuclear transloca
202 transiently tetramerized by the locally high thyroxine (T(4)) concentration, chaperoning it out into
205 pening of a cryptic pocket that accommodates thyroxine (T(4)) through an I Se halogen bond to Sec170
206 at catalyze the conversion of the prohormone thyroxine (T(4)) to the active form of thyroid hormone,
207 ect of NT69L on blood glucose, cortisol, and thyroxine (T(4)) were all back to control levels after f
208 sitive method for the analysis of six THs, l-thyroxine (T(4)), 3,3',5-triiodo-l-thyronine (T(3)), 3,3
209 id-stimulating hormone (TSH), free and total thyroxine (T(4)), and total reverse T(3) from baseline t
210 Thyroid-stimulating hormone (TSH), free thyroxine (T(4)), free triiodothyronine (T(3)), and lept
213 onine) with high affinity, and its precursor thyroxine (T(4), 3,5,3',5'-tetraiodo-l-thyronine) with l
214 ion of thyroid hormones triiodothyronine and thyroxine (T3/T4) can impact metabolism, body compositio
217 HFs whether TRH (30 nM), TSH (10 mU ml(-1)), thyroxine (T4) (100 nM), and triiodothyronine (T3) (100
219 asing log10 perchlorate and decreasing total thyroxine (T4) [regression coefficient (beta) = -0.70; 9
220 selenoenzyme that activates the pro-hormone thyroxine (T4) and supplies most of the 3,5,3'-triiodoth
222 tion, circulating levels of thyroid hormones thyroxine (T4) and triiodothyronine (T3) averaged 46.9 a
223 yroid, or thyroglobulin), which contain both thyroxine (T4) and triiodothyronine (T3), were the first
227 e thyroid hormones triiodothyronine (T3) and thyroxine (T4) in aquatic wildlife exists despite the fa
230 4.00 mU or more per liter and a normal free thyroxine (T4) level (0.86 to 1.90 ng per deciliter [11
231 boxylate transporter 8 (MCT8) have low serum thyroxine (T4) levels that cannot be fully explained by
232 m 3,5,3'-triiodothyronine (T3) with normal l-thyroxine (T4) levels, is associated with malignancy.
235 evidence suggests that the thyroid hormone L-thyroxine (T4) stimulates growth of cancer cells via a p
236 concentrations, either through inhibition of thyroxine (T4) synthesis or through inhibition of Dio me
237 es the type 2 deiodinase (D2) that activates thyroxine (T4) to 3,3',5-triiodothyronine (T3), the disr
238 elenoenzymes that catalyze the conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) and 3,3',
239 oidism involves the endogenous conversion of thyroxine (T4) to 3,5,3'-triiodothyronine (T3) and may n
243 pe II iodothyronine deiodinase (D2) converts thyroxine (T4) to the active hormone 3,5,3'-triiodothyro
244 pe 2 deiodinase (D2) converts the prohormone thyroxine (T4) to the metabolically active molecule 3,5,
245 zymes, such as TH deiodinases, which convert thyroxine (T4) to the physiologically active TH, triiodo
248 thyroid hormones (triiodothyronine (T3) and thyroxine (T4)), thyroid-stimulating hormone, thyroid pe
249 The thyroid hormones triiodothyronine (T3), thyroxine (T4), and thyrotropin (TSH) were measured in p
250 e examined through thyroid histology, plasma thyroxine (T4), and triiodothyronine (T3), and hepatic o
251 f the label by the natural thyroid hormone l-thyroxine (T4), as a model analyte, is demonstrated in w
253 oped for the analysis of the thyroid hormone thyroxine (T4), inflammation biomarker C-reactive protei
257 1 induced a dose-dependent increase in serum thyroxine (T4), with a maximum effect after 10 proportio
262 phytohaemagglutinin skin test, p < 0.0001), thyroxine (T4, p = 0.042), and glutathione (GSH, p = 0.0
263 eled T3 internal standard (T3-13C9), labeled thyroxine (T4-d5) is also added to serum samples in orde
264 ing vessels was increased 3-fold by either l-thyroxine (T4; 10(-7) mol/L) or 3,5,3'-triiodo-l-thyroni
265 membrane receptor, binds thyroid hormones (L-thyroxine, T4; 3,5,3'-triiodo-L-thyronine, T3) and is ov
267 l compartment to a hypertrophic regimen with thyroxine, the cartilage discs underwent progressive dee
268 e 2 deiodinase (D2), an enzyme that converts thyroxine, the main form of thyroid hormone in the circu
272 urrently reads "... for steady delivery of L-thyroxine").This has been corrected in the online versio
273 al thyroid hormone levels (thyrotropin, free thyroxine, thyroid peroxidase antibodies) were measured
274 time of 90 ms and allowed the amount of free thyroxine to be determined within 30 s after sample inje
275 thelial cell line, HLE B-3, was treated with thyroxine to determine whether this treatment increases
276 eiodinase (D2) that activates the prohormone thyroxine to the active hormone triiodothyronine, modify
277 activation by accelerating the conversion of thyroxine to triiodothyronine via type 2 deiodinase in m
278 ones (ie, thyroid-stimulating hormone, total thyroxine, total triiodothyronine, free thyroxine, free
281 ays of growth in a hyperoxic atmosphere, the thyroxine-treated cells were 20 times more viable than w
288 including thyroid-stimulating hormone (TSH), thyroxine, triiodothyronine resin uptake, and free thyro
289 compensate for thyroid dysfunction, as serum thyroxine/triiodothyronine and somatic growth were norma
290 zo-p-dioxins and furans, with THs [total (L)-thyroxine (TT(4)), total 3,3',5-triiodo-(L)-thyronine (T
291 d a 53% and 46% decline in circulating total thyroxine (TT4) and 3,5,3'-triiodothyronine (TT3), respe
292 of thyroid-stimulating hormone (TSH), total thyroxine (TT4), and PFAAs were measured during 2005-200
294 ips between thyroid hormones (total and free thyroxine [TT4 and FT4], total and free triiodothyronine
295 or Tiredness score modified the effects of L-thyroxine versus placebo (P for interaction = 0.20 and 0
297 imulating hormone, total thyroxine, and free thyroxine, were measured in serum samples collected betw
298 of the thyroid hormones triiodothyronine and thyroxine, which are required for the development of the
299 hypothyroidism is replacement with synthetic thyroxine, which undergoes peripheral conversion to trii
300 ions of thyroid-stimulating hormone and free thyroxine with the outcomes were assessed through logist