ライフサイエンスコーパス: TSH

1 TSH at baseline was not significantly associated with in

2 TSH concentrations decreased during hypoglycemia (P<0.01

3 TSH is composed of a alpha-subunit common to gonadotropi

4 TSH level was positively associated with QRS interval in

5 TSH levels followed a U-curve trend in early pregnancy w

6 TSH levels significantly affected the maximal keratometr

7 TSH levels were positively associated with Base of suppo

8 TSH stimulated translocation of beta-arrestin-1 and -2 t

9 TSH with portal vein occlusion is an established method

10 er MBq of (131)I administered, between the 2 TSH stimulation methods.

11 st one CRP dosage (13% three or more), 58% a TSH dosage (7%) and 8% a test for coeliac diseases (1%)

12 AM, and porin could be abolished by K1-70, a TSH-receptor antagonist, suggesting a TSH receptor-media

13 Further, we identified a TSH-like factor that may confer osteoprotection.

14 -70, a TSH-receptor antagonist, suggesting a TSH receptor-mediated action.

15 n California's Salinas Valley and abstracted TSH levels from their children's medical records.

16 ormation, and hyperresorption that accompany TSH deficiency.

17 Additionally, TSH regulates post-translational changes in thyroglobuli

18 Multivariable adjusted TSH, FT4 and T3 levels were 25%, 1.3% and 3.9% lower in

19 Moreover, Alexa546-TSH-activated TSHR internalization was not accompanied b

20 01), T4t (p < .001), T3t/T4t (P = .001), and TSH (p = .001) plasma levels.

21 which includes early involvement of ACTH and TSH and a relatively rapid development of hypopituitaris

22 TAS2R agonists also inhibited basal and TSH-dependent iodide efflux.

23 the manufacturers' methods for both FT4 and TSH has shown that the variability among immunoassays ca

24 As for FT4 and TSH levels, no significant distribution trend of myocard

25 es of the TSH receptor (TSHR) homodimer, and TSH-stimulated IP1 production (EC(50)=50 mU/ml) were ind

26 rum total T4 was measured by immunoassay and TSH was measured by chemiluminescent assay.

27 hormone (TSH)-dependent Ca(2+) increases and TSH-dependent iodide efflux in thyrocytes.

28 roxine and free-triiodothyronine levels, and TSH-receptor autoantibodies in patients with GD.

29 could be contained via p53-dependent OIS and TSH is a major disruptor of this balance.

30 ns between high exposure to several PFAS and TSH level in early gestations.

31 hormone (TSH) in women during pregnancy, and TSH in neonates.

32 sent with combined deficiency of GH, PRL and TSH.

33 Notably, as measured by calorimetry, T3 and TSH increased follicular heat production, whereas T3/T4

34 We categorized T4 and TSH into 7 groups with cut-offs at the 5(th), 20(th), 40

35 /DeltaID) Src-1(-/-) mice have normal TH and TSH levels and are triiodothryonine (T(3)) sensitive at

36 eam of thyroid-stimulating hormone (TSH) and TSH receptor (TSHR) and is indispensable for TSH/TSHR-me

37 ccording to the currently most reliable anti-TSH receptor antibody-ELISA used to diagnose Graves dise

38 Euthyroidism was defined as TSH of 0.45 to 4.49 mIU/L, subclinical hypothyroidism as

39 .9 mIU/L, and subclinical hyperthyroidism as TSH <0.45 mIU/L, the last two with normal free thyroxine

40 .49 mIU/L, and subclinical hypothyroidism as TSH 4.5 to 19.9 mIU/L with free thyroxine (fT4) levels w

41 to 4.49 mIU/L, subclinical hypothyroidism as TSH of 4.5 to 19.9 mIU/L, and subclinical hyperthyroidis

42 ions were not modified by infant sex, age at TSH measurement, maternal serum polychlorinated biphenyl

43 Cross-sectionally, AT TSH-beta (TSHB) mRNA was evaluated in 4 independent coho

44 ween any of the PFASs and changes of average TSH or fT4 levels in total samples.

45 lly elderly patients and those with baseline TSH levels below 10 mU/L.

46 in men, while a U-shape association between TSH and QRS was observed in women.

47 imed to investigate the relationship between TSH mRNA and cholesterol metabolism in human adipose tis

48 teric interaction site, NAM S37a blocks both TSH- and PAM-induced activation of the TSHR.

49 -effectiveness acceptability curves for both TSH stimulation methods and (131)I activities.

50 TSHR activation by TSH phosphorylates protein kinases AKT1, p38alpha, and E

51 Thyroid hormone synthesis is stimulated by TSH activating its receptor (TSHR), which upregulates th

52 In U2OS-TSHR cells, TSH up-regulated pAKT1 (7.1+/-0.5-fold), p38alpha (2.9+/

53 a dose-dependent manner, but did not change TSH levels, weight, histology, or expression of marker g

54 Negatively charged TSH-hydrazone ions furthermore show a simple and predict

55 Although circadian TSH secretion has been well documented, the mechanism of

56 enes during chronic elevation of circulating TSH.

57 the suprachiasmatic nucleus pacemaker, daily TSH secretion profiles are disrupted in some patients wi

58 ced total T4 in pregnant women and decreased TSH in male neonates.

59 iquid formulation with the same L-T4 dosage, TSH circulating levels were normalized.

60 ive L-T4 in tablets, maintaining the dosage, TSH levels worsened again reaching levels in the hypothy

61 ence and functional divergence of duplicated TSH beta-subunit paralogs (tshbetaa and tshbetab) in Atl

62 Golgi/TGN organization all impair efficient TSH-dependent cAMP response element binding protein (CRE

63 ent is the best diagnostic test; an elevated TSH level almost always signals primary hypothyroidism.

64 It is unclear to what extent the elevated TSH contributes to tumor progression.

65 internalization in thyroid cells, endogenous TSH receptors traffic retrogradely to the trans-Golgi ne

66 function by maternal melatonin and establish TSH signal transduction as a key substrate for the encod

67 ecific analyses, we found that the estimated TSH values were higher among the highest perfluorooctane

68 cluding DEC1, suppressing BMAL2 and the EYA3/TSH pathway, triggering winter biology.

69 y through the eyes absent/thyrotrophin (EYA3/TSH) pathway.

70 se cells under basal conditions or following TSH-stimulation.

71 For TSH, we identify a novel variant in SYN2 (MAF=23.5%, P=6

72 .65 (95% confidence interval, 0.84-3.23) for TSH of 7.0 to 9.9 mIU/L, 1.86 (95% confidence interval,

73 .01 (95% confidence interval, 0.81-1.26) for TSH of 4.5 to 6.9 mIU/L, 1.65 (95% confidence interval,

74 pulations into the same category was 65% for TSH and MUIC, and 83% for TSH and goiter prevalence.

75 .94 (95% confidence interval, 1.01-3.72) for TSH <0.10 mIU/L (P for trend=0.047).

76 .86 (95% confidence interval, 1.27-2.72) for TSH of 10.0 to 19.9 mIU/L (P for trend <0.01) and 1.31 (

77 tegory was 65% for TSH and MUIC, and 83% for TSH and goiter prevalence.

78 .31 (95% confidence interval, 0.88-1.95) for TSH of 0.10 to 0.44 mIU/L and 1.94 (95% confidence inter

79 (odds ratio (OR) per standard deviation for TSH 1.05, 95% confidence interval (CI) 0.97 to 1.12; for

80 TSH receptor (TSHR) and is indispensable for TSH/TSHR-mediated proliferation of thyroid follicular ce

81 identify 74 genome-wide significant loci for TSH, of which 28 are previously unreported.

82 igher and lower TSH levels, particularly for TSH >/=10 and <0.10 mIU/L.

83 Dose responses for TSH-stimulated dissociation of prebound (125)I-TSH (nega

84 an approach to harmonization of results for TSH.

85 We found TSH-induced phosphorylation of these kinases in 2 cell l

86 L-, inhibited ACTH- and did not alter LH/FSH/TSH-release; and 3) resistin increased ACTH-release and

87 ed ACTH-release and did not alter PRL/LH/FSH/TSH-secretion.

88 levels of free triiodothyronine (FT3), FT4, TSH, and TPOAb were measured.

89 Furthermore, TSH increased expression of osteoblast marker genes ALPL

90 a clinical laboratory-based third-generation TSH immunoassay.

91 Within the DTC group, TSH level was predictive for cardiovascular mortality; t

92 A high TSH dose (100 mU/ml) caused a 33% decrease in cell-surfa

93 diated by G(s) and G(i)/G(o) at low and high TSH doses, respectively, which may represent a mechanism

94 affect the decreased cAMP production at high TSH doses, we studied the roles of TSHR downregulation a

95 ic dose-response curve that plateaus at high TSH doses.

96 to Gs at low TSH doses and to G(i/o) at high TSH doses.

97 ently stimulate cAMP signaling and at higher TSH concentrations to acutely stimulate phosphoinositide

98 ed variants and a polygenic score for higher TSH levels is associated with a reduced risk of thyroid

99 ables suggests a protective effect of higher TSH levels (indicating lower thyroid function) on risk o

100 er longevity has been associated with higher TSH and lower TH levels, but mechanisms underlying TSH/T

101 was defined as thyroid-stimulating hormone (TSH) 0.45 to 4.49 mIU/L, and subclinical hypothyroidism

102 noassays, using thyroid stimulating hormone (TSH) and 17beta-estradiol (E2) as model analytes, respec

103 ons of maternal thyroid-stimulating hormone (TSH) and free thyroxine (fT4) levels with plasma concent

104 ating levels of thyroid stimulating hormone (TSH) and thyroid hormone (TH) in an inverse relationship

105 s downstream of thyroid-stimulating hormone (TSH) and TSH receptor (TSHR) and is indispensable for TS

106 echolamines nor thyroid-stimulating hormone (TSH) are responsible for sarcolipin expression or FAO st

107 on with newborn thyroid-stimulating hormone (TSH) concentration >5 mIU/L, median urinary iodine conce

108 ined as a serum thyroid-stimulating hormone (TSH) concentration greater than the pregnancy-specific r

109 Since thyroid-stimulating hormone (TSH) exerts an inductor effect on cholesterol biosynthes

110 with antihuman thyroid stimulating hormone (TSH) IgG molecules and the detection of TSH antigens wer

111 one (ACTH), and thyroid stimulating hormone (TSH) in both normal and tumor tissues can be assessed by

112 lamus (MBH) and thyroid-stimulating hormone (TSH) in the pituitary.

113 , total T4, and thyroid-stimulating hormone (TSH) in women during pregnancy, and TSH in neonates.

114 Thyroid stimulating hormone (TSH) is critical for normal development and metabolism.

115 i-quantitative thyr oid stimulating hormone (TSH) lateral flow immunochromatographic assays (LFA) are

116 ined as a serum thyroid-stimulating hormone (TSH) level of 5.0 to 19.96 mIU/l with normal total thyro

117 ons between low thyroid-stimulating hormone (TSH) levels and high bone turnover markers, low bone min

118 onal control of thyroid-stimulating hormone (TSH) levels as well as neuromodulatory functions.

119 e (TH) and high thyroid-stimulating hormone (TSH) levels in the serum, is strongly associated with no

120 d with maternal thyroid-stimulating hormone (TSH) levels.

121 ormone (TH) and thyroid-stimulating hormone (TSH) levels.

122 Serum thyroid-stimulating hormone (TSH) measurement is the best diagnostic test; an elevate

123 onal reserve of thyroid-stimulating hormone (TSH) production and the TSH set point later in life.

124 nt of the serum thyroid-stimulating hormone (TSH) radioimmunoassay led to the discovery that many pat

125 ies against the thyroid-stimulating hormone (TSH) receptor.

126 ly regulated by thyroid-stimulating hormone (TSH) secretion within the hypothalamic-pituitary-thyroid

127 ent for the two thyroid-stimulating hormone (TSH) stimulation methods (thyroid hormone withdrawal [TH

128 oxine (fT4) and thyroid stimulating hormone (TSH) was measured.

129 y expression of thyroid-stimulating hormone (TSH), an increase in the blood concentration of thyroid

130 Plasma free T4, thyroid-stimulating hormone (TSH), and 8 am cortisol levels were normal.

131 ncentrations of thyroid-stimulating hormone (TSH), and autoantibodies to thyroperoxidase (ATPO) in re

132 hyroxine (FT4), thyroid-stimulating hormone (TSH), and thyroid peroxidase antibody (TPOAb) were obtai

133 yroid function [thyroid-stimulating hormone (TSH), free and total thyroxine (fT4, TT4) and triiodothy

134 ations of serum thyroid-stimulating hormone (TSH), free and total thyroxine (T(4)), and total reverse

135 cally predicted thyroid stimulating hormone (TSH), free thyroxine (FT4) and thyroid peroxidase antibo

136 ncentrations of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and thyroglobulin, vary wide

137 rolactin (PRL), thyroid stimulating hormone (TSH), free triiodothyronine (fT3), and free thyroxin (fT

138 Serum levels of thyroid-stimulating hormone (TSH), total thyroxine (TT4), and PFAAs were measured dur

139 sensitivity to thyroid stimulating hormone (TSH), which is dramatically and persistently increased b

140 , however, that thyroid-stimulating hormone (TSH), which is low in most hyperthyroid states, directly

141 tively regulate thyroid-stimulating hormone (TSH)-dependent Ca(2+) increases and TSH-dependent iodide

142 1, 2013, from a thyroid-stimulating hormone (TSH)-receptor antibody (TRAb) test register in south Wal

143 LXRs activated thyroid-stimulating hormone (TSH)-releasing hormone (TRH)-positive neurons in the par

144 levels of serum thyroid-stimulating hormone (TSH).

145 3), free T4, or thyroid-stimulating hormone (TSH).

146 zation of serum thyroid-stimulating hormone (TSH).

147 e Plus (DP) and thyroid-stimulating hormone (TSH).

148 in response to thyroid-stimulating hormone (TSH).

149 (Anti-TPO), and thyroid stimulating hormone (TSH).

150 he thyrotropin [thyroid-stimulating hormone (TSH)] receptor (TSHR) is known to acutely and persistent

151 elation between thyroid-stimulating hormone (TSH; also known as thyrotropin) level and these outcome

152 ct of different thyroid-stimulation hormone (TSH) levels.

153 [TT3 and FT3], thyroid-stimulating hormone [TSH], and thyroglobulin [Tg]) and levels of Pb, Hg, and

154 vels of estradiol (E2) and thyroid hormones (TSH, T3t, T4t) were also determined.

155 rmone withdrawal [THW] and recombinant human TSH [rhTSH]) and the two iodine-131 ((131)I) activities

156 In addition, recombinant human TSH alpha/beta administration resulted in increased HMGC

157 H-stimulated dissociation of prebound (125)I-TSH (negative cooperativity; EC(50)=70 mU/ml), which req

158 = 0.656; I(2): 87.58%) while an elevation in TSH levels was observed (WMD: 0.248 mIU/L, 95% CI: 0.001

159 linical significance, if any, of the rise in TSH is unclear.

160 n variants explain >/=20% of the variance in TSH and FT4.

161 al testosterone and PRL levels and increased TSH levels.

162 east one nonagenarian sibling have increased TSH secretion but similar bioactivity of TSH and similar

163 d from cells previously exposed to increased TSH, a TSHR agonist, a cAMP analog, or a TSHR-stimulatin

164 Knockdown of beta-arrestin-1 inhibited TSH-stimulated up-regulation of mRNAs for OPN by 87 +/-

165 e agonist and a neutral antagonist inhibited TSH-stimulated persistent IP1 production, whereas the in

166 lation of beta-arrestin-1 by siRNA inhibited TSH-stimulated phosphorylation of ERK1/2, p38alpha, and

167 ich is what has been observed upon injecting TSH.

168 The large TSH-bound ectodomain of the thyrotropin receptor (TSHR)

169 ) Leptin stimulated PRL/ACTH/FSH- but not LH/TSH-release; 2) adiponectin stimulated PRL-, inhibited A

170 s initiated by binding of the hormone ligand TSH to the ECD.

171 aints within the ECD of the TSHR, its ligand TSH, and the hormone-receptor complex.

172 0.15 (95% CI: -0.28, -0.03) lower serum log(TSH)mIU/L with adjustment for covariates.

173 ngs in patients with hyperthyroidism are low TSH, elevated free-thyroxine and free-triiodothyronine l

174 ling of the TSH receptor (TSHR) to Gs at low TSH doses and to G(i/o) at high TSH doses.

175 ile and estimated ORs for binary high or low TSH and fT4 status based on the week-specific distributi

176 Persistently low TSH concentrations at 1 year after diagnosis were associ

177 peculate that TNFalpha elevations due to low TSH signaling in human hyperthyroidism contribute to the

178 In order to determine whether low TSH levels contribute to bone loss in hyperthyroidism, w

179 A lower TSH level is associated with increased cardiovascular mo

180 ts were increased with both higher and lower TSH levels (P for quadratic pattern <0.01); the hazard r

181 ts were increased with both higher and lower TSH levels, particularly for TSH >/=10 and <0.10 mIU/L.

182 for each 10-fold decrease in geometric mean TSH level.

183 he LFA format, however, is unable to measure TSH in the normal range or detect suppressed levels of T

184 ncreased cAMP levels stimulated by 100 mU/ml TSH from 55% to 73% of the peak level.

185 difference in cAMP levels at 1 and 100 mU/ml TSH.

186 nsignificant inverse relations with neonatal TSH.

187 ultured human scalp HFs whether TRH (30 nM), TSH (10 mU ml(-1)), thyroxine (T4) (100 nM), and triiodo

188 d NCoRDeltaID, have low TH levels and normal TSH.

189 af(V600E)-induced PTC (BVE-PTC) under normal TSH, we transplanted BVE-PTC tumors subcutaneously into

190 yroxinemia as fT4<5th percentile with normal TSH.

191 uals, higher circulating fT4 levels, but not TSH levels, are associated with increased risk of incide

192 e, thereby demonstrating that the absence of TSH signaling contributes to bone loss.

193 gical studies identifying a direct action of TSH on the skeleton.

194 Here we show that the skeletal actions of TSH deficiency are mediated, in part, through TNFalpha.

195 revealed an inverted U-shaped association of TSH (p < 0.001), but no association of FT4 concentration

196 The association of TSH levels in the euthyroid and subclinical hypothyroid

197 sed TSH secretion but similar bioactivity of TSH and similar TH levels compared to controls.

198 and enhances the synthesis and biopotency of TSH, the hormone secreted by thyrotropes.

199 iation between outcomes and concentration of TSH using Cox regression and outcomes and free thyroxine

200 one (TSH) IgG molecules and the detection of TSH antigens were employed to demonstrate high protein i

201 h increasing cAMP production at low doses of TSH and decreased cAMP production at high doses (>1 mU/m

202 bank demonstrates the pleiotropic effects of TSH-associated variants and a polygenic score for higher

203 indings highlight the pleiotropic effects of TSH-associated variants on thyroid function and growth o

204 However, the direct influence of TSH on the osteoblast has remained unclear.

205 athogenic TSHR Abs measured by inhibition of TSH binding to the TSHR.

206 ollicular cells was due to the inhibition of TSH-mediated activation of the mTOR complex 1/ribosomal

207 normal range or detect suppressed levels of TSH (<0.4 mIU L(-1); hyperthyroidism).

208 TSHR to mediate responses at lower levels of TSH and that decreased cAMP production at high doses may

209 nerally confirm the expected binding mode of TSH to the ECD as well as the general fold of the domain

210 or rapid and point-of-care quantification of TSH using a cell phone.

211 Quantification of TSH was performed in an iOS application directly on the

212 T4-mediated negative feedback regulation of TSH expression.

213 first in vitro study of NCOR1 regulation of TSH in a physiologically relevant cell system, the Talph

214 We demonstrate biphasic regulation of TSH-mediated cAMP production involving coupling of the T

215 study identifies GLIS3 as a key regulator of TSH/TSHR-mediated thyroid hormone biosynthesis and proli

216 ypothalamus and thus stimulated secretion of TSH from the pituitary.

217 in mice with wild-type TshR, suppression of TSH did not revert the phenotype.

218 dies suggest that therapeutic suppression of TSH to very low levels may contribute to bone loss in pe

219 PRL (P<0.01) were lower while the values of TSH (P = 0.02), fT3 (P = 0.08), and fT4 (P = 0.04) were

220 m the Rotterdam Study with data available on TSH (thyroid-stimulating hormone), FT4 (free thyroxine)

221 r TSHR/C41S heterodimers could only bind one TSH, TSH-stimulated IP1 production was decreased relativ

222 uded and randomized to resection by ALPPS or TSH, with the option of rescue ALPPS in the TSH group, i

223 ferred to as thyroid-stimulating hormone, or TSH) level with normal levels of free thyroxine (FT4) af

224 t adjuvant enhanced the levels of pathogenic TSH-binding inhibition and thyroid-stimulating Abs, as w

225 The increased amount of pituitary TSH was caused by reduced expression of type 2 iodothyro

226 This locally produced TSH suppresses osteoclast formation in a negative feedba

227 gold nanoparticles on an LFA for quantifying TSH levels.

228 s able to provide point-of-care quantitative TSH results with a high level of sensitivity and reprodu

229 Obtaining quantitative TSH results, especially in the low concentration range,

230 In fact, it does not provide quantitative TSH values at all.

231 yroid hormones and only very modestly raises TSH levels, the clinical significance, if any, of the ri

232 nists for thyrocyte-expressed TAS2Rs reduced TSH-dependent Ca(2+) release in Nthy-Ori 3-1 cells, but

233 ngenital central hypothyroidism with reduced TSH biopotency, over-secretion of FSH at neonatal minipu

234 A concentrations was associated with reduced TSH in boys (-9.9% per log2 unit; 95% CI: -15.9%, -3.5%)

235 ssor, NCOR1, has been postulated to regulate TSH expression, presumably by interacting with thyroid h

236 perativity; EC(50)=70 mU/ml), which requires TSH binding to both sites of the TSH receptor (TSHR) hom

237 The resulting TSH-hydrazones are separated by ultrahigh-performance li

238 Our findings reveal TSH as a circannual output of the PT, which in turn regu

239 efined subclinical hypothyroidism as a serum TSH between 5 and 10 mIU/L, and overt hypothyroidism as

240 0 mIU/L, and overt hypothyroidism as a serum TSH greater than 10 mIU/L, but this is not the commonly

241 Euthyroidism was defined as a serum TSH level of 0.47 to 4.9 mIU/l.

242 thyroxine should be started to achieve serum TSH concentrations within the reference ranges for pregn

243 subclinical and antibody-negative) and serum TSH concentration.

244 range for each laboratory value, or by serum TSH concentrations greater than 2.5 mIU/L in the first t

245 ic assays (LFA) are used to screen for serum TSH concentration >5 mIUL(-1) (hypothyroidism).

246 d an approximately 3-fold elevation in serum TSH levels and a 40% reduction in biological activity.

247 to liquid oral formulation normalised serum TSH levels, and that switching back to tablets caused th

248 We estimated the percentage changes of serum TSH and fT4 levels according to concentrations (in nanog

249 the importance of rigorous control of serum TSH in PTC patients.

250 are symptom relief and maintenance of serum TSH levels within the reference range.

251 However, normalization of serum TSH with L-T4 monotherapy results in relatively low seru

252 monotherapy at doses to normalize the serum TSH became the standard of care.

253 hyroidism despite normalization of the serum TSH has been identified.

254 /L, 95% CI 2.68-3.62; p<0.0001), while serum TSH concentrations decreased from 2.91 mU/L (SD 1.68) to

255 s in XPA/FOXE1 (TTF-2) associated with serum TSH (p = 5.5E-08 to 1.0E-09); a nonsynonymous SNP (p = 1

256 factor scores were not associated with serum TSH, TgAb, or TPOAb.

257 xpression in FRTL5 cells modify the specific TSH response.

258 r, we contrasted the estimated week-specific TSH or fT4 levels by PFAS quartile and estimated ORs for

259 Thyroid Association guidelines of tempering TSH suppression in patients with low risk of cancer recu

260 We conclude that TSH enhances osteoblast differentiation in U2OS cells th

261 novel study provides little indication that TSH, FT4 or TPOAb positivity affects IHD, despite potent

262 x vivo bone marrow cell cultures showed that TSH inhibits and stimulates TNFalpha production from mac

263 We present data suggesting that TSH-stimulated TG phosphorylation contributes to enhance

264 The TSH effects on MTCO1, TFAM, and porin could be abolished

265 The TSH marker had a sensitivity of 0.75 and specificity of

266 The TSH marker has a better agreement with goiter prevalence

267 stimulating hormone (TSH) production and the TSH set point later in life.

268 Mutations in the genes encoding the TSH receptor (TSHR) or the Gs protein alpha subunit (GNA

269 TSH, with the option of rescue ALPPS in the TSH group, if the criteria for volume increase was not m

270 The sensitivity and specificity of the TSH marker was determined against MUIC and goiter preval

271 ch requires TSH binding to both sites of the TSH receptor (TSHR) homodimer, and TSH-stimulated IP1 pr

272 ed cAMP production involving coupling of the TSH receptor (TSHR) to Gs at low TSH doses and to G(i/o)

273 Thyrotropin (TSH) activation of the TSH receptor (TSHR), a 7-transmembrane-spanning receptor

274 ng iodine status in the population using the TSH marker and either MUIC or goiter prevalence in schoo

275 g the iodine status of populations using the TSH marker is warranted.

276 Thyrotropin (TSH) activation of the TSH receptor (TSHR), a 7-transmem

277 pin-releasing hormone (TRH) and thyrotropin (TSH), are expressed in human hair follicles (HFs) and re

278 addressed the potential role of thyrotropin (TSH).

279 astritis, who showed high serum thyrotropin (TSH) levels (in the hypothyroid range) while in therapy

280 In this study we report that thyrotropin (TSH) and the pathogenic, GD-specific monoclonal autoanti

281 The thyrotropin (TSH) receptor (TSHR) signals via G proteins of all four

282 athogenic autoantibodies to the thyrotropin (TSH) receptor (TSHR), can be treated but not cured.

283 or the heritable thyroid traits thyrotropin (TSH) and free thyroxine (FT4), we analyse whole-genome s

284 l thyroid function tests (serum thyrotropin [TSH], free thyroxine [fT4], and thyroid peroxidase [TPO]

285 th thyroid hormone receptors (THRs) bound to TSH subunit genes.

286 etter understand the genetic contribution to TSH levels, we conduct a GWAS meta-analysis at 22.4 mill

287 ed with 26 months for patients randomized to TSH (P = 0.028).

288 he liver, and also 28 patients randomized to TSH (P = 0.028).

289 80% (39 patients) for patients randomized to TSH (P = 0.091), including rescue ALPPS.

290 ivatization with p-toluenesulfonylhydrazine (TSH).

291 tination are an inherent property of the TRH/TSH feedback mechanism and indicate that only constant d

292 R/C41S heterodimers could only bind one TSH, TSH-stimulated IP1 production was decreased relative to

293 a location comparable to the pars tuberalis TSH cells involved in seasonal physiology and behaviour

294 d lower TH levels, but mechanisms underlying TSH/TH differences and longevity remain unknown.

295 Two-sample Mendelian randomization using TSH index variants as instrumental variables suggests a

296 To determine whether TSH signaling cooperates with oncogenic Braf in this pro

297 r common variants (MAF>/=1%) associated with TSH and FT4 (N=16,335).

298 shift in serum PFOA was not associated with TSH or TT4 levels in all children combined.

299 tients with CRLM and sFLR <30% compared with TSH.

300 uman thyrocyte cultures hyperstimulated with TSH also showed an increased intrinsic ability to form T