ライフサイエンスコーパス: thyroid-stimulating hormone

1 les should prompt measurement of circulating thyroid-stimulating hormone.

2 rates, and levels of C-reactive protein and thyroid-stimulating hormone.

3 e exposures under study were associated with thyroid-stimulating hormone.

4 gene, in primary thyroid cells treated with thyroid-stimulating hormone.

5 dine kinetics as seen with recombinant human thyroid-stimulating hormone.

6 f patients, and 12% developed elevated serum thyroid-stimulating hormone.

7 mone (LH), chorionic gonadotropin (hCG), and thyroid-stimulating hormone.

8 of 948 case-control pairs were assessed for thyroid-stimulating hormone.

9 CT after administration of recombinant human thyroid-stimulating hormone.

10 range or slightly decreased concentration of thyroid-stimulating hormone.

11 alysis to euthyroid participants (defined by thyroid-stimulating hormone 0.4-4.0 mIU/L).

12 ate of (124)I PET/CT after recombinant human thyroid-stimulating hormone (124)I PET/CT as implemented

13 Thyroid-stimulating hormone administration led to a vari

14 We show here that negative regulation of the thyroid-stimulating hormone alpha (TSHalpha) promoter by

15 In contrast, the thyroid-stimulating hormone alpha-subunit (TSH alpha) ge

16 ee negatively regulated genes (the pituitary thyroid-stimulating hormone alpha-subunit [TSH alpha], T

17 us nonhuman hormones we have developed human thyroid stimulating hormone and chorionic gonadotropin a

18 TC risk stratification have emerged, such as thyroid stimulating hormone and molecular markers.

19 of thyroxine, reverse triiodothyronine, and thyroid-stimulating hormone and a decrease in serum trii

20 crease in 3,5,3'-triiodothyronine (T(3)) and thyroid-stimulating hormone and an increase in reverse T

21 Associations of thyroid-stimulating hormone and free thyroxine with the

22 iodine supplementation on maternal or infant thyroid-stimulating hormone and free thyroxine.

23 We assessed the association of thyroid-stimulating hormone and FT4 with the risk of SCD

24 to reduced mRNA expression of both pituitary thyroid-stimulating hormone and hypothalamic thyrotropin

25 ct correlation between circulating levels of thyroid-stimulating hormone and NIS expression in vivo w

26 All patients had normal levels of thyroid-stimulating hormone and no other gastrointestina

27 nlarged follicles, in the presence of normal thyroid-stimulating hormone and T4 hormone levels.

28 nce of NCOR1DeltaID, the abnormally elevated thyroid-stimulating hormone and TH levels found in Thrb(

29 hat express both alpha- and beta-subunits of thyroid-stimulating hormone and the transcription factor

30 amily that includes luteinzing hormone (LH), thyroid stimulating hormone, and chorionic gonadotropin.

31 r three analytes (prostate specific antigen, thyroid stimulating hormone, and luteinizing hormone) we

32 era were assayed for thyroid autoantibodies, thyroid-stimulating hormone, and anti-FcepsilonRIalpha a

33 ormone family including luteinizing hormone, thyroid-stimulating hormone, and chorionic gonadotropin.

34 tudy resembles those reported for prolactin, thyroid-stimulating hormone, and free fatty acids.

35 ctin, cortisol, adrenocorticotropic hormone, thyroid-stimulating hormone, and free thyroxine levels.

36 -specific regulation of growth hormone (GH), thyroid-stimulating hormone, and prolactin (PRL) secreti

37 ficient mice, thyrotropin-releasing hormone, thyroid-stimulating hormone, and thyroid hormone are dec

38 As part of the study, plasma selenium, thyroid-stimulating hormone, and total and free T(3) and

39 ty lipoprotein cholesterol, creatine kinase, thyroid-stimulating hormones, and erythrocyte sedimentat

40 ement procedures for serum concentrations of thyroid-stimulating hormone are likewise under developme

41 human fetal pituitary cultures, where GH and thyroid-stimulating hormone are mediated by both SSTR2 a

42 ds of a glycoprotein using recombinant human thyroid-stimulating hormone as a model system.

43 hormone-releasing hormone tests or sensitive thyroid-stimulating hormone assays.

44 Thyroxine, free thyroxine index, and thyroid-stimulating hormone at 6 mo were inversely assoc

45 increase heart weight or decrease pituitary thyroid-stimulating hormone beta (TSHbeta) expression.

46 ligand-dependent negative regulation of the thyroid-stimulating hormone beta (TSHbeta) gene.

47 d repress the alpha glycoprotein subunit and thyroid-stimulating hormone beta promoters.

48 We found that thyroid-stimulating hormone beta subunit (tshb) and type

49 0th and 12th cysteine (Cys88-Cys105 in human thyroid-stimulating hormone beta-subunit (hTSHbeta)) of

50 Growth hormone, prolactin, and thyroid-stimulating hormone beta-subunit expression were

51 ollicle-stimulating hormone beta-subunit and thyroid-stimulating hormone beta-subunit) showed no sign

52 ere was selective expression of the gene for thyroid-stimulating hormone beta; detection of the thyro

53 5% CI: -0.092, -0.013), and increasing log10 thyroid-stimulating hormone (beta = 0.071; 95% CI: 0.008

54 erse events were observed, and elevations of thyroid-stimulating hormone, blood urea nitrogen, and cr

55 r pituitary cells that express the genes for thyroid-stimulating hormone but not in the cells that ex

56 s bind to the receptor and mimic its ligand, thyroid stimulating hormone, causing the characteristic

57 on, growth hormone, luteinizing hormone, and thyroid-stimulating hormone cells and tumors had the hig

58 marrow, liver, and renal function; and serum thyroid-stimulating hormone concentration lower than 0.5

59 tween examinations, age, sex, baseline serum thyroid-stimulating hormone concentration, and cystic co

60 mmendations are based on the degree to which thyroid-stimulating hormone concentrations have deviated

61 al T(4) (TT(4)), total triiodothyronine, and thyroid-stimulating hormone concentrations were compared

62 an thyroid cells by the activation of serum, thyroid-stimulating hormone/cyclic AMP, or epidermal gro

63 iciency (12.5%), precocious puberty (12.2%), thyroid-stimulating hormone deficiency (9.2%), and thyro

64 rated that FRTL-5 cells express megalin in a thyroid-stimulating hormone-dependent manner.

65 unting for persistently reduced secretion of thyroid-stimulating hormone despite low plasma thyroid h

66 a, it is unclear which individuals with mild thyroid-stimulating hormone elevations will benefit from

67 leptin-induced thyrotropin-releasing hormone/thyroid-stimulating hormone expression.

68 Thyroid stimulating hormone, free thyroxine, 25-hydroxy

69 Rotterdam Study with data available on TSH (thyroid-stimulating hormone), FT4 (free thyroxine) and g

70 agnosed based on baseline blood sampling for thyroid stimulating hormone, gonadotropin, and prolactin

71 Thyroid stimulating hormone (h(2)=0.58, P=2 x 10(-)(5))

72 ein, low-density lipoprotein, triglycerides, thyroid stimulating hormone, homocysteine, C-reactive pr

73 idines that bind with high-affinity to human thyroid stimulating hormone (hTSH) were isolated from a

74 modeling we have designed recombinant human thyroid-stimulating hormone (hTSH) analogs with increase

75 The human thyroid-stimulating hormone (hTSH) subunits alpha and be

76 design of experiments (DOE) optimization for thyroid-stimulating hormone immunoassays, varying (1) th

77 of (131)I within lesions, and of the role of thyroid-stimulating hormone in stimulating the sodium-io

78 s of serum thyroxin, and augmented levels of thyroid-stimulating hormone in the pituitary gland), fea

79 id not differ among the four groups, whereas thyroid-stimulating hormone increased upon iodine supple

80 il domain of STRN and to a kinase-dependent, thyroid-stimulating hormone-independent proliferation of

81 ytes, suggesting that a relevant part of the thyroid-stimulating hormone-induced proliferation signal

82 mplexes for sulfated glycopeptides of equine thyroid stimulating hormone is compared with information

83 We have previously shown that thyroid-stimulating hormone is required, but not suffici

84 Hematocrit level, thyroid stimulating hormone level, autoimmune antibody l

85 hyroid hormone withdrawal to achieve a serum thyroid-stimulating hormone level in excess of 30 microI

86 t hypothyroxinemia without markedly lowering thyroid stimulating hormone levels, thus creating a bioc

87 proximately 50-80%) and profoundly increased thyroid-stimulating hormone levels ( approximately 800-1

88 Tg-BRAF2 and Tg-BRAF3 mice had increased thyroid-stimulating hormone levels (>7- and approximatel

89 e interval, 1.68-3.47 per 1 ng/dL) and lower thyroid-stimulating hormone levels (hazard ratio, 0.92;

90 ) per genetically predicted 1 SD decrease in thyroid-stimulating hormone levels and 1.05 (95% CI, 1.0

91 Genetically predicted thyroid-stimulating hormone levels and hyperthyroidism w

92 rb(PV/PV) mice exhibit highly elevated serum thyroid-stimulating hormone levels and increased TH.

93 suggested that subclinical abnormalities in thyroid-stimulating hormone levels are associated with d

94 idence for a causal association of decreased thyroid-stimulating hormone levels in the direction of a

95 For subclinical hypothyroidism (based on thyroid-stimulating hormone levels of 4.1 to 11.0 mIU/L)

96 Subclinical thyroid dysfunction, defined as thyroid-stimulating hormone levels outside the reference

97 s aged 65 years or older with baseline serum thyroid-stimulating hormone levels were enrolled in 1989

98 c variant in GNAS associating with increased thyroid-stimulating hormone levels when maternally inher

99 Long-term, 5 patients developed elevated thyroid-stimulating hormone levels, 5 were diagnosed wit

100 blood cell count, C-reactive protein levels, thyroid-stimulating hormone levels, and thyroid peroxida

101 , most HTNs are seen in patients with normal thyroid-stimulating hormone levels.

102 ished cAMP-Epac-mediated Rap1 activation and thyroid-stimulating hormone-mediated cell proliferation,

103 aled that activation of Epac is required for thyroid-stimulating hormone or cAMP stimulation of DNA s

104 ts from the Rotterdam Study >/=45 years with thyroid-stimulating hormone or free thyroxine (FT4) meas

105 tected no changes in serum concentrations of thyroid-stimulating hormone or free tri-iodothyronine, f

106 which competitively inhibits the binding of thyroid-stimulating hormone or the human autoantibody to

107 The elevation of thyroid-stimulating hormone, or thyrotropin (TSH), that

108 ated serum thyrotropin (often referred to as thyroid-stimulating hormone, or TSH) level with normal l

109 ormone levels and inappropriate thyrotropin (thyroid-stimulating hormone, or TSH) production.

110 after therapy was associated with response (thyroid-stimulating hormone, P2 =.01; free T4, P2 =.0049

111 luded left ventricular dysfunction, elevated thyroid stimulating hormone, palmar-plantar erythrodyses

112 nce to suggest that high doses that suppress thyroid stimulating hormone prevent disease recurrence i

113 l nervous system (locomotion) and endocrine (thyroid-stimulating hormone, prolactin and insulin secre

114 ith lung metastases when a recombinant human thyroid-stimulating hormone protocol is used.

115 cium, intact parathyroid hormone (iPTH), and thyroid stimulating hormone; psychological symptom inven

116 had no effect on fasting-induced changes in thyroid-stimulating hormone pulsatility, thyroid and IGF

117 ecretion, as well as luteinizing hormone and thyroid-stimulating hormone pulsitility.

118 Genetic associations of the thyroid stimulating hormone receptor (TSHR) gene with GD

119 s12101255 and rs12101261) in intron 1 of the thyroid stimulating hormone receptor (TSHR) gene.

120 The thyroid stimulating hormone receptor (TSHR) is a G prote

121 onal outcome is predicted for over a hundred thyroid stimulating hormone receptor (TSHR) mutations, a

122 The thyroid stimulating hormone receptor (TSHR) represents t

123 The roles of the thyroid stimulating hormone receptor and cellular and hu

124 nformations that were created by joining the thyroid stimulating hormone receptor exoloops constraine

125 sociated with human brittle bone disease and thyroid stimulating hormone receptor hyperactivity.

126 ceptor/follicle stimulating hormone receptor/thyroid stimulating hormone receptor were mapped using e

127 verexpression and showed decreased levels of thyroid stimulating hormone receptor-stimulating Abs and

128 s II-restricted autoantibody response to the thyroid stimulating hormone receptor.

129 duction of stimulating autoantibodies to the thyroid-stimulating hormone receptor (TSHR) (TSAbs) that

130 Tg and the thyroid-stimulating hormone receptor (TSHR) are targets

131 Thyroid-stimulating hormone receptor (TSHR) expression i

132 The thyroid-stimulating hormone receptor (TSHR) is a G prote

133 high homology with LHCGR, we predicted that thyroid-stimulating hormone receptor (TSHR) might be act

134 m because of autoantibodies that bind to the thyroid-stimulating hormone receptor (TSHR) on the thyro

135 Thyroid-stimulating hormone receptor (TSHR) plays a cent

136 hyroidism is caused by autoantibodies to the thyroid-stimulating hormone receptor (TSHR) that act as

137 tors (luteinizing hormone receptor (LHR) and thyroid-stimulating hormone receptor (TSHR)) was expecte

138 The thyrotropin receptor, also known as the thyroid-stimulating hormone receptor (TSHR), is the prim

139 at the luteinizing hormone receptor and the thyroid-stimulating hormone receptor (TSHR), stimulation

140 The genes for thyroid-stimulating hormone receptor (TSHR), the SOX11 t

141 pin receptor (LHCGR) and the closely related thyroid-stimulating hormone receptor (TSHR), was fundame

142 odium iodide symporter, thyroperoxidase, and thyroid-stimulating hormone receptor and to a moderate a

143 levels and coordinating the expression of a thyroid-stimulating hormone receptor antagonist (TSHAnta

144 dies to thyroperoxidase or thyroglobulin, or thyroid-stimulating hormone receptor antibodies (TRAbs),

145 to the agonist and antagonist activities of thyroid-stimulating hormone receptor autoantibodies.

146 gion or in p10 can inhibit activation of the thyroid-stimulating hormone receptor by autoantibodies.

147 Thyroid-stimulating hormone receptor expressing cells al

148 Expression of functional thyroid-stimulating hormone receptor in the skin may hav

149 We found significant expression of the thyroid-stimulating hormone receptor mRNA in cultured ke

150 at these tissues share a common antigen: the thyroid-stimulating hormone receptor protein.

151 The presence of thyroid-stimulating hormone receptor was confirmed by no

152 r was confirmed by northern analyses and the thyroid-stimulating hormone receptor was found to be fun

153 roid differentiation markers, thyroglobulin, thyroid-stimulating hormone receptor, thyroid peroxidase

154 o be linked to photoperiod and reproduction (thyroid-stimulating hormone receptor, TSHR).

155 ations at Ser-281 in the hinge region of the thyroid-stimulating hormone receptor, we mutated the con

156 unit GPA2, serves as a second ligand for the thyroid-stimulating hormone receptor.

157 uction of stimulating antibodies against the thyroid-stimulating hormone receptor.

158 thyroid, but in states of hyperactivation of thyroid-stimulating hormone receptors (TSHRs), patients

159 tion mutants of luteinizing hormone (LH) and thyroid-stimulating hormone receptors found in patients

160 suppressive if suppression was documented by thyroid-stimulating hormone-releasing hormone tests or s

161 We now report that thyroid-stimulating hormone represses mitogen-activated

162 r production of growth hormone, prolactin or thyroid-stimulating hormone, resulting in dysmorphogenes

163 neck dissection and use of recombinant human thyroid stimulating hormone (rhTSH) for (1)(3)(1)I radio

164 atients with injections of recombinant human thyroid-stimulating hormone (rhTSH) and thyroid hormone

165 ormone withdrawal (THW) or recombinant human thyroid-stimulating hormone (rhTSH) injections before (1

166 each prepared with either recombinant human thyroid-stimulating hormone (rhTSH) or thyroid hormone w

167 or with administration of recombinant human thyroid-stimulating hormone (rhTSH).

168 current findings of using recombinant human thyroid-stimulating hormone (rhTSH, also known as Thyrog

169 tion for remnant ablation (recombinant human thyroid-stimulating hormone [rhTSH] vs. traditional thyr

170 contemporary use of recombinant thyrotropin (thyroid-stimulating hormone) (rTSH) to prepare patients

171 inopathy was cost-effective as compared with thyroid-stimulating hormone screening.

172 Hyperthyroidism due to thyroid-stimulating hormone-secreting tumors accounts fo

173 sium channel subunits KCNQ1 and KCNE2 form a thyroid-stimulating hormone-stimulated, constitutively a

174 Thyroid-stimulating hormone stimulates proliferation thr

175 rum biomarkers of thyroid function including thyroid-stimulating hormone, thyroglobulin, total and fr

176 (triiodothyronine (T3) and thyroxine (T4)), thyroid-stimulating hormone, thyroid peroxidase antibodi

177 g RRA after preparation by recombinant human thyroid-stimulating hormone (thyrotropin; TSH) over the

178 These compounds, as well as thyroid-stimulating hormone, total thyroxine, and free t

179 The 11 analytes included 9 hormones (ie, thyroid-stimulating hormone, total thyroxine, total trii

180 n, stimulates DNA synthesis in quiescent and thyroid-stimulating hormone-treated thyrocytes.

181 sessable patients have developed an elevated thyroid-stimulating hormone; treatment with thyroxine ha

182 petitive and competitive immunoassays, using thyroid stimulating hormone (TSH) and 17beta-estradiol (

183 t AKAP121 protein expression is regulated by thyroid stimulating hormone (TSH) and cAMP.

184 d (HPT) axis maintains circulating levels of thyroid stimulating hormone (TSH) and thyroid hormone (T

185 itu modification of pCB films with antihuman thyroid stimulating hormone (TSH) IgG molecules and the

186 GH), adrenocorticotropic hormone (ACTH), and thyroid stimulating hormone (TSH) in both normal and tum

187 nsible for deficiencies of GH, prolactin and thyroid stimulating hormone (TSH) in Snell and Jackson d

188 Thyroid stimulating hormone (TSH) is critical for normal

189 The established function of thyroid stimulating hormone (TSH) is to promote thyroid

190 tion of autoantibodies against receptors for thyroid stimulating hormone (TSH) on thyroid epithelial

191 utoantibody and its Fab fragment bind to the thyroid stimulating hormone (TSH) receptor (TSHR) with h

192 15 months; necropsy was performed and serum thyroid stimulating hormone (TSH) was measured.

193 odothyronine (fT3), free thyroxine (fT4) and thyroid stimulating hormone (TSH) was measured.

194 It has long been known that thyroid stimulating hormone (TSH), a central component o

195 k factors according to genetically predicted thyroid stimulating hormone (TSH), free thyroxine (FT4)

196 ions of total testosterone, prolactin (PRL), thyroid stimulating hormone (TSH), free triiodothyronine

197 Thyroid Stimulating Hormone (TSH), T3 and T4 levels were

198 ng effect depends on tanycyte sensitivity to thyroid stimulating hormone (TSH), which is dramatically

199 thyroid peroxidase antibody (Anti-TPO), and thyroid stimulating hormone (TSH).

200 The euthyroid state was defined as thyroid-stimulating hormone (TSH) 0.45 to 4.49 mIU/L, an

201 yroidism is defined as an elevation in serum thyroid-stimulating hormone (TSH) above the upper limit

202 ional-week specific associations of maternal thyroid-stimulating hormone (TSH) and free thyroxine (fT

203 roid hormone associated with nonsuppressible thyroid-stimulating hormone (TSH) and impaired growth.

204 value and correlated to the available serum thyroid-stimulating hormone (TSH) and thyroid peroxidase

205 we demonstrate that GLIS3 acts downstream of thyroid-stimulating hormone (TSH) and TSH receptor (TSHR

206 Neither catecholamines nor thyroid-stimulating hormone (TSH) are responsible for sa

207 In this issue of Cell, identify thyroid-stimulating hormone (TSH) as an important regula

208 pha-subunit (alphaSU)-null mice that develop thyroid-stimulating hormone (TSH) cell hyperplasia with

209 icated by >3% of the population with newborn thyroid-stimulating hormone (TSH) concentration >5 mIU/L

210 ha (TRalpha(o/o)) that maintain normal serum thyroid-stimulating hormone (TSH) concentration despite

211 hyroidism, and is usually defined as a serum thyroid-stimulating hormone (TSH) concentration greater

212 ne (T4) and T3, and modest or no increase in thyroid-stimulating hormone (TSH) concentration.

213 Thyroid-stimulating hormone (TSH) controls thyroid growt

214 The cumulative incidence of GHD, thyroid-stimulating hormone (TSH) deficiency, adrenocort

215 streamlined, we evaluated the time course of thyroid-stimulating hormone (TSH) elevation after total

216 Since thyroid-stimulating hormone (TSH) exerts an inductor eff

217 ed sensitive assays for thyroid hormones and thyroid-stimulating hormone (TSH) has increased identifi

218 Thyroid-stimulating hormone (TSH) has long been recogniz

219 RH) in the mediobasal hypothalamus (MBH) and thyroid-stimulating hormone (TSH) in the pituitary.

220 measured free thyroxine (T4), total T4, and thyroid-stimulating hormone (TSH) in women during pregna

221 A 15-min stimulation with thyroid-stimulating hormone (TSH) led to an activation o

222 SCH was defined as a serum thyroid-stimulating hormone (TSH) level of 5.0 to 19.96

223 ted to achieve a normal and suppressed serum thyroid-stimulating hormone (TSH) level, respectively.

224 inical data showing correlations between low thyroid-stimulating hormone (TSH) levels and high bone t

225 reported condition characterized by elevated thyroid-stimulating hormone (TSH) levels and normal free

226 Serum thyroxine, T3, and thyroid-stimulating hormone (TSH) levels and pituitary T

227 hyroid function through suppression of serum thyroid-stimulating hormone (TSH) levels and TSH-beta su

228 Controlled treatment studies that used thyroid-stimulating hormone (TSH) levels as an inclusion

229 opeptide that exerts the hormonal control of thyroid-stimulating hormone (TSH) levels as well as neur

230 ities have been uncommon except for elevated thyroid-stimulating hormone (TSH) levels found in approx

231 yroid hormone levels, and none have measured thyroid-stimulating hormone (TSH) levels in neonates.

232 terized by low thyroid hormone (TH) and high thyroid-stimulating hormone (TSH) levels in the serum, i

233 Patients with serum thyroid-stimulating hormone (TSH) levels outside the ref

234 ent were collected, and thyroxine (T(4)) and thyroid-stimulating hormone (TSH) levels were measured a

235 tary adrenocorticotrophic hormone (ACTH) and thyroid-stimulating hormone (TSH) levels were normal, bu

236 elevated serum TH and inappropriately normal thyroid-stimulating hormone (TSH) levels, consistent wit

237 ons were positively associated with maternal thyroid-stimulating hormone (TSH) levels.

238 aracterized by high thyroid hormone (TH) and thyroid-stimulating hormone (TSH) levels.

239 Serum thyroid-stimulating hormone (TSH) measurement is the bes

240 Following analysis of serial thyroid-stimulating hormone (TSH) measurements collected

241 We recently described the direct effects of thyroid-stimulating hormone (TSH) on bone and suggested

242 m implications for the functional reserve of thyroid-stimulating hormone (TSH) production and the TSH

243 al practice: 1) The development of the serum thyroid-stimulating hormone (TSH) radioimmunoassay led t

244 We have shown recently that by acting on the thyroid-stimulating hormone (TSH) receptor (TSHR), TSH n

245 of wild type or N54-alpha(s) along with the thyroid-stimulating hormone (TSH) receptor and adenylyl

246 Use of human FSH/thyroid-stimulating hormone (TSH) receptor chimeras sugg

247 The thyroid-stimulating hormone (TSH) receptor signals via G

248 GD is caused by autoantibodies against the thyroid-stimulating hormone (TSH) receptor.

249 yrotropin-releasing hormone (TRH) stimulates thyroid-stimulating hormone (TSH) secretion from the ant

250 with controls infused with vehicle, whereas thyroid-stimulating hormone (TSH) secretion was not chan

251 rculating TH levels are tightly regulated by thyroid-stimulating hormone (TSH) secretion within the h

252 hibitor of pituitary growth hormone (GH) and thyroid-stimulating hormone (TSH) secretion, binds to fi

253 oid ablation rate was equivalent for the two thyroid-stimulating hormone (TSH) stimulation methods (t

254 tropin-releasing hormone (TRH) and pituitary thyroid-stimulating hormone (TSH) subunit genes, however

255 Plasma thyroid-stimulating hormone (TSH) was significantly supp

256 Thyroid-stimulating hormone (TSH), a central neuroendocr

257 oid follicular cells, a system that requires thyroid-stimulating hormone (TSH), acting via cAMP, to m

258 d an increase in the pituitary expression of thyroid-stimulating hormone (TSH), an increase in the bl

259 Plasma free T4, thyroid-stimulating hormone (TSH), and 8 am cortisol lev

260 e thyroiditis (AIT), serum concentrations of thyroid-stimulating hormone (TSH), and autoantibodies to

261 ternal serum levels of free thyroxine (FT4), thyroid-stimulating hormone (TSH), and thyroid peroxidas

262 e shown that the anterior pituitary hormone, thyroid-stimulating hormone (TSH), can bypass the thyroi

263 rometry, and biomarkers of thyroid function [thyroid-stimulating hormone (TSH), free and total thyrox

264 ints were changes in concentrations of serum thyroid-stimulating hormone (TSH), free and total thyrox

265 iomarkers, including serum concentrations of thyroid-stimulating hormone (TSH), free thyroxine (FT4),

266 Thyroid-stimulating hormone (TSH), free thyroxine (T(4))

267 A panel of thyroid measures, including thyroid-stimulating hormone (TSH), thyroxine, triiodothy

268 Serum levels of thyroid-stimulating hormone (TSH), total thyroxine (TT4)

269 There is evidence, however, that thyroid-stimulating hormone (TSH), which is low in most

270 Also, thyroid-stimulating hormone (TSH), which is released by

271 thyroidal Na(+)/I(-) symporter expression is thyroid-stimulating hormone (TSH)-dependent and basolate

272 ods and pharmaceuticals, negatively regulate thyroid-stimulating hormone (TSH)-dependent Ca(2+) incre

273 protein levels are dynamically regulated in thyroid-stimulating hormone (TSH)-dependent thyroid cell

274 Thyroid-stimulating hormone (TSH)-induced reduction in l

275 etween Jan 1, 1998, and Dec 31, 2013, from a thyroid-stimulating hormone (TSH)-receptor antibody (TRA

276 Depletion of LXRs activated thyroid-stimulating hormone (TSH)-releasing hormone (TRH

277 Thyroid-stimulating hormone (TSH)-secreting tumors (TSH-

278 drenocorticotropin hormone (ACTH)-secreting, thyroid-stimulating hormone (TSH)-secreting, and nonfunc

279 ), Rab1b expression increases in response to thyroid-stimulating hormone (TSH).

280 to be a primary source of intestine-derived thyroid-stimulating hormone (TSH).

281 ), and between anti-Dechlorane Plus (DP) and thyroid-stimulating hormone (TSH).

282 evelop PTC rapidly with high levels of serum thyroid-stimulating hormone (TSH).

283 ith total triiodothyronine (T3), free T4, or thyroid-stimulating hormone (TSH).

284 ine (L-T4) along with normalization of serum thyroid-stimulating hormone (TSH).

285 The thyrotropin [thyroid-stimulating hormone (TSH)] receptor (TSHR) is kn

286 Evidence was presented that thyrotropin [thyroid-stimulating hormone (TSH)]-stimulated persistent

287 e mortality and explore the relation between thyroid-stimulating hormone (TSH; also known as thyrotro

288 Recent studies have identified a role for thyroid-stimulating hormone (TSH; ie, thyrotropin) as an

289 e, heterodimeric glycoprotein hormones, like thyroid-stimulating hormone (TSH; thyrotropin), have onl

290 tal and free triiodothyronine [TT3 and FT3], thyroid-stimulating hormone [TSH], and thyroglobulin [Tg

291 1), alanine aminotransferase (p = 0.035) and thyroid-stimulating hormone values (p = 0.013) than thos

292 xample, only a small number of patients with thyroid-stimulating hormone values of more than 10 mIU/L

293 [OR] 5.78, 95% CI 2.00-16.67; p=0.001), and thyroid stimulating hormone was increased on average by

294 in the ISP56 group, and the concentration of thyroid-stimulating hormone was higher in the ISP90 grou

295 Thyroid-stimulating hormone was measured in sera obtaine

296 At the last follow-up visit, thyroid-stimulating hormone was similar in both groups.

297 Thyroid-stimulating hormone was suppressed in patients g

298 a (free thyroxine </=10th percentile, normal thyroid-stimulating hormone) was associated with an incr

299 , free thyroxine, free triiodothyronine, and thyroid-stimulating hormone were measured in 1996 (n = 9

300 id cancer (DTC) may be prepared using either thyroid-stimulating hormone withdrawal (THW) or recombin