ライフサイエンスコーパス: stimulating hormone

1 slightly decreased concentration of thyroid-stimulating hormone.

2 s of adrenocorticotropin or alpha-melanocyte-stimulating hormone.

3 ld prompt measurement of circulating thyroid-stimulating hormone.

4 ive effects of [Nle, D-Phe]-alpha-melanocyte-stimulating hormone.

5 and levels of C-reactive protein and thyroid-stimulating hormone.

6 agouti-related protein and alpha-melanocyte stimulating hormone.

7 proopiomelanocortin-derived alpha-melanocyte-stimulating hormone.

8 ion with its natural ligand alpha-melanocyte-stimulating hormone.

9 case-control pairs were assessed for thyroid-stimulating hormone.

10 administration of recombinant human thyroid-stimulating hormone.

11 tenedione, luteinizing hormone, and follicle-stimulating hormone.

12 o euthyroid participants (defined by thyroid-stimulating hormone 0.4-4.0 mIU/L).

13 124)I PET/CT after recombinant human thyroid-stimulating hormone (124)I PET/CT as implemented in this

14 tro and in vivo data of new alpha-melanocyte-stimulating hormone (alpha-MSH) analogues which are N-te

15 g in selective increases of alpha-melanocyte-stimulating hormone (alpha-Msh) and carboxy-cleaved beta

16 ted release of anorexigenic alpha-melanocyte stimulating hormone (alpha-MSH) and orexigenic Agouti-re

17 C4R responds to an agonist, alpha-melanocyte-stimulating hormone (alpha-MSH) and to an antagonist/inv

18 the neuroprotective peptide alpha-melanocyte stimulating hormone (alpha-MSH) attenuates GABAergic los

19 K2 increased the release of alpha-melanocyte-stimulating hormone (alpha-MSH) from ex vivo hypothalami

20 revealed that both NPY and alpha-melanocyte-stimulating hormone (alpha-MSH) inhibit and stimulate, r

21 alpha-Melanocyte stimulating hormone (alpha-MSH) is a neuropeptide that s

22 The neuropeptide alpha-melanocyte stimulating hormone (alpha-MSH) is an important regulato

23 te-suppressing neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) is reduced, yet the mRNA

24 ed at revealing the role of alpha-melanocyte-stimulating hormone (alpha-MSH) on basophil function.

25 We report that melanocyte-stimulating hormone (alpha-MSH) or ACTH induce ATR-pS435

26 eled lactam bridge-cyclized alpha-melanocyte-stimulating hormone (alpha-MSH) peptide on its melanoma-

27 ed and X-Ala-Asp-conjugated alpha-melanocyte stimulating hormone (alpha-MSH) peptides.

28 abeled Arg-X-Asp-conjugated alpha-melanocyte stimulating hormone (alpha-MSH) peptides.

29 nd the POMC-derived peptide alpha-melanocyte-stimulating hormone (alpha-MSH) promote satiety.

30 eptor (MC1R), also known as alpha-melanocyte-stimulating hormone (alpha-MSH) receptor, is an attracti

31 n of MC1R in melanocytes by alpha-melanocyte-stimulating hormone (alpha-MSH) stimulates cAMP signalli

32 xypeptidase (PRCP) degrades alpha-melanocyte-stimulating hormone (alpha-MSH) to an inactive form that

33 ypothalamus (PVN), to block alpha-melanocyte-stimulating hormone (alpha-MSH) type 3 and 4 receptors,

34 ing the alpha-melanocortin (alpha-melanocyte-stimulating hormone (alpha-MSH))-induced increase in the

35 tractant protein-1 (MCP-1), alpha-melanocyte stimulating hormone (alpha-MSH), and peroxisome prolifer

36 ng release of products like alpha-melanocyte-stimulating hormone (alpha-MSH), neuropeptide Y (NPY), g

37 ts, melanotan-II (MT-II) or alpha-melanocyte stimulating hormone (alpha-MSH), were unilaterally micro

38 eceptor to bind its ligand, alpha-melanocyte-stimulating hormone (alpha-MSH).

39 and lesional skin levels of alpha-melanocyte-stimulating hormone (alpha-MSH).

40 ce of stimulation by the agonist, melanocyte-stimulating hormone (alpha-MSH).

41 euron-derived MC4R agonist, alpha-melanocyte stimulating hormone (alpha-MSH).

42 anorexigenic neuromodulator alpha-melanocyte-stimulating hormone (alpha-MSH; referred to here as alph

43 hypothalamic Pomc mRNA and alpha-melanocyte-stimulating hormone (alphaMSH) peptide levels were marke

44 hysiologically activated by alpha-melanocyte stimulating hormone (alphaMSH), MC1R function can be ant

45 e, densities of AgRP- and alpha-melanocortin stimulating hormone (alphaMSH)-immunoreactive fibers wer

46 cAMP levels in response to alpha-melanocyte-stimulating hormone, an MC4R agonist, by blocking ligand

47 e safety and efficacy of an alpha-melanocyte-stimulating hormone analogue, afamelanotide, to decrease

48 peptides alpha-, beta-, and gamma-melanocyte-stimulating hormone and ACTH are full agonists for all o

49 ing superovulation with recombinant follicle-stimulating hormone and administration of gonadotropin-r

50 n 3,5,3'-triiodothyronine (T(3)) and thyroid-stimulating hormone and an increase in reverse T(3).

51 opiomelanocortin-derived peptides melanocyte-stimulating hormone and corticotropin.

52 Furthermore, an increase in follicle-stimulating hormone and decreases in testosterone and th

53 Associations of thyroid-stimulating hormone and free thyroxine with the outcomes

54 We assessed the association of thyroid-stimulating hormone and FT4 with the risk of SCD by usin

55 was associated with decreased serum follicle-stimulating hormone and higher claudin-11 expression alo

56 ed mRNA expression of both pituitary thyroid-stimulating hormone and hypothalamic thyrotropin-releasi

57 e in detail effects on secretion of follicle-stimulating hormone and luteinising hormone.

58 ody mass index (P = .05), and lower follicle-stimulating hormone and luteinizing hormone (each P < .0

59 We measured follicle-stimulating hormone and luteinizing hormone and added in

60 Pituitary gonadotropins follicle-stimulating hormone and luteinizing hormone are heterodi

61 e further found that WNT5a prevents follicle-stimulating hormone and luteinizing protein from up-regu

62 in melanocytes, mediated by alpha-melanocyte-stimulating hormone and melanin-concentrating hormone, r

63 stratification have emerged, such as thyroid stimulating hormone and molecular markers.

64 crophages, we observed that alpha-melanocyte-stimulating hormone and selective MC1-R agonists similar

65 to spermatozoa, whereas recombinant follicle-stimulating hormone and steroid hormones are ineffective

66 COR1DeltaID, the abnormally elevated thyroid-stimulating hormone and TH levels found in Thrb(PV) mice

67 ell-permeable peptide, a hormone (melanocyte stimulating hormone), and a blood-clotting agent can be

68 assayed for thyroid autoantibodies, thyroid-stimulating hormone, and anti-FcepsilonRIalpha antibodie

69 rtisol, adrenocorticotropic hormone, thyroid-stimulating hormone, and free thyroxine levels.

70 nth analysis evaluated E2, E1, E1S, follicle-stimulating hormone, and luteinizing hormone levels in a

71 analytes (prostate specific antigen, thyroid stimulating hormone, and luteinizing hormone) were print

72 ical activity, luteinizing hormone, follicle-stimulating hormone, and progesterone.

73 th the anorexigenic peptide alpha-melanocyte-stimulating hormone, and the opioid peptide beta-endorph

74 rotein cholesterol, creatine kinase, thyroid-stimulating hormones, and erythrocyte sedimentation rate

75 Follicle-stimulating hormone, anti-Mullerian hormone, and inhibin

76 ocedures for serum concentrations of thyroid-stimulating hormone are likewise under development.

77 the density of anorexigenic alpha-melanocyte-stimulating hormone axons was reduced in adult Magel2-nu

78 P, rs11031006, in the region of the follicle-stimulating hormone B polypeptide (FSHB) gene strongly a

79 We found that thyroid-stimulating hormone beta subunit (tshb) and type 2 deiod

80 from the hypothalamus and regulates follicle-stimulating hormone beta-subunit (FSHbeta) gene expressi

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

82 th sex hormone-binding globulin and follicle-stimulating hormone (beta = -0.04, 95% confidence interv

83 0.092, -0.013), and increasing log10 thyroid-stimulating hormone (beta = 0.071; 95% CI: 0.008, 0.133)

84 Increased levels of follicle-stimulating hormone (beta = 0.20, 95% confidence interva

85 g levels of luteinizing hormone and follicle-stimulating hormone but apparently normal responsiveness

86 o the receptor and mimic its ligand, thyroid stimulating hormone, causing the characteristic clinical

87 liver, and renal function; and serum thyroid-stimulating hormone concentration lower than 0.5 mIU/L.

88 iables: age, body-mass index, basal follicle-stimulating hormone concentration, and the number of pre

89 ons are based on the degree to which thyroid-stimulating hormone concentrations have deviated from no

90 adiol, the free estradiol index, or follicle-stimulating hormone concentrations.

91 stosterone, luteinizing hormone, or follicle-stimulating hormone concentrations.

92 Results for estradiol and follicle-stimulating hormone confirmed the results based on statu

93 he endogenous MC4R agonist alpha-melanoctyte-stimulating hormone course parallel and wrap around ante

94 ifferent molecular sizes, [d-Trp]-melanocyte-stimulating hormone, [d-Ala]-deltorphin, [d-Phe]-achatin

95 (12.5%), precocious puberty (12.2%), thyroid-stimulating hormone deficiency (9.2%), and thyroidal hyp

96 ce, but it does not restore alpha-melanocyte-stimulating hormone-dependent cAMP signaling.

97 eled lactam bridge-cyclized alpha-melanocyte stimulating hormone derivative, betaAlaNleCycMSH(hex).

98 or persistently reduced secretion of thyroid-stimulating hormone despite low plasma thyroid hormone.

99 nduced thyrotropin-releasing hormone/thyroid-stimulating hormone expression.

100 Thyroid stimulating hormone, free thyroxine, 25-hydroxy vitamin

101 n erythropoietin (hEPO) is an erythropoiesis stimulating hormone frequently employed in antianemia th

102 n hormones (luteinizing hormone and follicle-stimulating hormone) from the pituitary.

103 Follicle stimulating hormone (FSH) acts through receptors (FSHR)

104 Serum follicle-stimulating hormone (FSH) and E2 were measured at baseli

105 of menses and serial monitoring of follicle-stimulating hormone (FSH) and inhibin A and B levels.

106 Although both the levels of follicle-stimulating hormone (FSH) and inhibin B are correlated w

107 productive physiology by regulating follicle-stimulating hormone (FSH) and luteinizing hormone (LH) g

108 itor of prostaglandin signaling and follicle-stimulating hormone (FSH) and luteinizing hormone (LH) s

109 ulates the pituitary gonadotropin's follicle-stimulating hormone (FSH) and luteinizing hormone (LH),

110 elease of the gonadotropic hormones follicle-stimulating hormone (FSH) and luteinizing hormone (LH),

111 and secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH),

112 osterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and sex hormone-binding globul

113 Follicle-stimulating hormone (FSH) and syt-9 are highly co-locali

114 , we briefly outline the roles that follicle-stimulating hormone (FSH) and testosterone play in regul

115 le interactions exist between human follicle-stimulating hormone (FSH) and the N-terminal hormone-bin

116 he preceding 6 months and levels of follicle-stimulating hormone (FSH) in the postmenopausal range.

117 ta-subunit of the pituitary hormone follicle-stimulating hormone (Fsh) increases bone mass in mice.

118 Follicle-stimulating hormone (FSH) is an essential regulator of g

119 d on evidence that the GPCR agonist follicle-stimulating hormone (FSH) promotes the protein kinase A

120 Follitropin, or follicle-stimulating hormone (FSH) receptor (FSHR), is a G protei

121 of transcription, androgens enhance follicle-stimulating hormone (FSH) receptor expression, which the

122 In adult humans, the follicle-stimulating hormone (FSH) receptor is expressed only in

123 Follicle-stimulating hormone (FSH) regulates follicular growth an

124 vation of protein kinase A (PKA) by follicle stimulating hormone (FSH) transduces the signal that dri

125 vel of antimullerian hormone (AMH), follicle-stimulating hormone (FSH), and inhibin B and urinary lev

126 the synthesis of the gonadotropins, follicle-stimulating hormone (FSH), and luteinizing hormone (LH).

127 sures of ovarian reserve were day-3 follicle-stimulating hormone (FSH), antral follicle count (AFC),

128 s innervation was observed close to follicle-stimulating hormone (FSH), luteinizing hormone (LH) and

129 (DHEAS), luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin, fasting plasma glu

130 rone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH), which were measured < or =8 t

131 lation, and thus, the expression of follicle-stimulating hormone (FSH)- and testosterone-induced targ

132 ian cancer nor its interaction with follicle-stimulating hormone (FSH)-driven proliferation in ovaria

133 mones, luteinizing hormone (LH) and follicle stimulating hormone (FSH).

134 essing luteinizing hormone (LH) and follicle-stimulating hormone (FSH)], with adrenocorticomelanotrop

135 emature ovarian failure (POF) rate (follicle-stimulating hormone [FSH] >/= 40 IU/L) after 1 year of f

136 The beta subunit of follicle stimulating hormone (FSHB) is expressed specifically in

137 am Study with data available on TSH (thyroid-stimulating hormone), FT4 (free thyroxine) and gait, wit

138 Reductions in levels of the hunger-stimulating hormone ghrelin have been proposed to mediat

139 refore investigated the role of the appetite-stimulating hormone ghrelin in olfactory processing in r

140 ression driving the production of the growth-stimulating hormone gibberellic acid and downstream grow

141 based on baseline blood sampling for thyroid stimulating hormone, gonadotropin, and prolactin deficie

142 Thyroid stimulating hormone (h(2)=0.58, P=2 x 10(-)(5)) and immu

143 gamma-MSH (gamma-melanocyte-stimulating hormone, H-Tyr-Val-Met-Gly-His-Phe-Arg-Trp-A

144 rived from the beta-domain of human Follicle-Stimulating Hormone (hFSH) are described.

145 -density lipoprotein, triglycerides, thyroid stimulating hormone, homocysteine, C-reactive protein an

146 f experiments (DOE) optimization for thyroid-stimulating hormone immunoassays, varying (1) the analyt

147 atus and in levels of estradiol and follicle-stimulating hormone in 2,659 women followed in the Study

148 um thyroxin, and augmented levels of thyroid-stimulating hormone in the pituitary gland), features fo

149 n of STRN and to a kinase-dependent, thyroid-stimulating hormone-independent proliferation of thyroid

150 In cultured hypothalamic neurons, melanocyte stimulating hormone induces an MC4R-dependent and sustai

151 ortin (POMC) that is processed to melanocyte-stimulating hormone, inducing tanning.

152 We have previously shown that thyroid-stimulating hormone is required, but not sufficient to i

153 amelanotide, an analogue of alpha-melanocyte-stimulating hormone, is known to induce tanning of the s

154 nd testicular weight, testosterone, follicle-stimulating hormone level, and luteinizing hormone level

155 Hematocrit level, thyroid stimulating hormone level, autoimmune antibody level, er

156 ely 50-80%) and profoundly increased thyroid-stimulating hormone levels ( approximately 800-1000-fold

157 al, 1.68-3.47 per 1 ng/dL) and lower thyroid-stimulating hormone levels (hazard ratio, 0.92; confiden

158 ) mice exhibit highly elevated serum thyroid-stimulating hormone levels and increased TH.

159 subclinical hypothyroidism (based on thyroid-stimulating hormone levels of 4.1 to 11.0 mIU/L), 1 fair

160 vier menstrual bleeding, and higher follicle-stimulating hormone levels were associated with longer m

161 and tandem mass spectrometry assay; follicle-stimulating hormone levels were measured at baseline and

162 t in GNAS associating with increased thyroid-stimulating hormone levels when maternally inherited.

163 ll count, C-reactive protein levels, thyroid-stimulating hormone levels, and thyroid peroxidase antib

164 yroxinemia without markedly lowering thyroid stimulating hormone levels, thus creating a biochemical

165 ed using anti-Mullerian hormone and follicle-stimulating hormone levels, was similar in both groups.

166 ings (insulin-like growth factor 1, follicle-stimulating hormone, luteinizing hormone, and testostero

167 ther by the agonistic MC1R ligand melanocyte stimulating hormone (MSH) or by pharmacologic cAMP induc

168 Melanocyte-stimulating hormone (MSH) plays a crucial role in pigmen

169 Melanocyte-stimulating hormone (MSH) reduces UV-induced DNA damage

170 C) receptor agonist DTrp(8)-gamma-melanocyte stimulating hormone (MSH; DTrp).

171 ists [alpha-, beta-, and gamma(2)-melanocyte stimulating hormones (MSH) and adrenocorticotropin (ACTH

172 such as alpha-, beta-, and gamma2-melanocyte stimulating hormones (MSH) and adrenocorticotropin hormo

173 [Nle(4),d-Phe(7)]-alpha-melanocyte-stimulating hormone (NDP-alpha-MSH) labeled with Eu(III)

174 protein (AGRP)/[Nle4,DPhe7]alpha-melanocyte stimulating hormone (NDP-MSH) ligands is reported.

175 ffect of [Nle(4), D-Phe(7)]-alpha-melanocyte stimulating hormone (NDP-MSH), a potent non-steroidogeni

176 the bound ligand [Nle(4),D-Phe(7)]melanocyte-stimulating hormone (NDP-MSH), thereby differentiating b

177 de glutamic acid-isoleucine/alpha-melanocyte-stimulating hormone (NEI/alphaMSH) peptides.

178 he FMP in the log rate of change of follicle-stimulating hormone (odds ratio, 0.65; 95% CI, 0.46-0.91

179 the Rotterdam Study >/=45 years with thyroid-stimulating hormone or free thyroxine (FT4) measurements

180 o changes in serum concentrations of thyroid-stimulating hormone or free tri-iodothyronine, free tetr

181 ompetitively inhibits the binding of thyroid-stimulating hormone or the human autoantibody to TSHR.

182 ft ventricular dysfunction, elevated thyroid stimulating hormone, palmar-plantar erythrodysesthesia,

183 eled lactam bridge-cyclized alpha-melanocyte-stimulating hormone peptides.

184 ease compared to KP10 and increased follicle-stimulating hormone plasma concentration.

185 pared from 7B2 null mice restored melanocyte-stimulating hormone production, substantiating the role

186 eatment with R-spondin2, similar to follicle stimulating hormone, promoted the development of primary

187 stimulation with the letrozole and follicle-stimulating hormone protocol preserves fertility in wome

188 tact parathyroid hormone (iPTH), and thyroid stimulating hormone; psychological symptom inventories (

189 Follicle-stimulating hormone receptor (FSHR), a G-protein coupled

190 in a classical pigmentation gene, melanocyte stimulating hormone receptor (MC1R), is strongly associa

191 of stimulating autoantibodies to the thyroid-stimulating hormone receptor (TSHR) (TSAbs) that induce

192 Tg and the thyroid-stimulating hormone receptor (TSHR) are targets for auto

193 Genetic associations of the thyroid stimulating hormone receptor (TSHR) gene with GD and GO

194 5 and rs12101261) in intron 1 of the thyroid stimulating hormone receptor (TSHR) gene.

195 The thyroid stimulating hormone receptor (TSHR) is a G protein-coupl

196 come is predicted for over a hundred thyroid stimulating hormone receptor (TSHR) mutations, as well a

197 e of autoantibodies that bind to the thyroid-stimulating hormone receptor (TSHR) on the thyroid gland

198 The thyroid stimulating hormone receptor (TSHR) represents the prima

199 teinizing hormone receptor (LHR) and thyroid-stimulating hormone receptor (TSHR)) was expected to be

200 The genes for thyroid-stimulating hormone receptor (TSHR), the SOX11 transcrip

201 dide symporter, thyroperoxidase, and thyroid-stimulating hormone receptor and to a moderate accumulat

202 and coordinating the expression of a thyroid-stimulating hormone receptor antagonist (TSHAntag), whic

203 thyroperoxidase or thyroglobulin, or thyroid-stimulating hormone receptor antibodies (TRAbs), or a co

204 agonist and antagonist activities of thyroid-stimulating hormone receptor autoantibodies.

205 in p10 can inhibit activation of the thyroid-stimulating hormone receptor by autoantibodies.

206 ons that were created by joining the thyroid stimulating hormone receptor exoloops constrained throug

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

208 ollicle stimulating hormone receptor/thyroid stimulating hormone receptor were mapped using exoloop-s

209 ferentiation markers, thyroglobulin, thyroid-stimulating hormone receptor, thyroid peroxidase, and so

210 ked to photoperiod and reproduction (thyroid-stimulating hormone receptor, TSHR).

211 ssion and showed decreased levels of thyroid stimulating hormone receptor-stimulating Abs and frequen

212 melanoma through targeting of the melanocyte-stimulating hormone receptor.

213 ops of luteinizing hormone receptor/follicle stimulating hormone receptor/thyroid stimulating hormone

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

215 ases beta-endorphin but not alpha-melanocyte-stimulating hormone release in the hypothalamus, and sys

216 before light onset, whereas alpha-melanocyte stimulating hormone release, especially at the end of th

217 receptor binding with the agonist melanocyte-stimulating hormone resulted in an increased proportion

218 with injections of recombinant human thyroid-stimulating hormone (rhTSH) and thyroid hormone withdraw

219 section and use of recombinant human thyroid stimulating hormone (rhTSH) for (1)(3)(1)I radioactive i

220 ithdrawal (THW) or recombinant human thyroid-stimulating hormone (rhTSH) injections before (131)I adm

221 findings of using recombinant human thyroid-stimulating hormone (rhTSH, also known as Thyrogen) as a

222 remnant ablation (recombinant human thyroid-stimulating hormone [rhTSH] vs. traditional thyroid horm

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

224 Hyperthyroidism due to thyroid-stimulating hormone-secreting tumors accounts for 1% of

225 sed luteinizing hormone relative to follicle-stimulating hormone secretion, insulin resistance and de

226 progesterone, luteinizing hormone, follicle-stimulating hormone, sex hormone-binding globulin, F(2)-

227 ocortin analog [Nle, D-Phe]-alpha-melanocyte-stimulating hormone (starting 3 or 6 hrs after injury) i

228 , hepatocyte growth factor, alpha-melanocyte stimulating hormone, stem cell factor, and fibroblast gr

229 nnel subunits KCNQ1 and KCNE2 form a thyroid-stimulating hormone-stimulated, constitutively active, t

230 ough follicles responded to initial follicle-stimulating hormone stimulation and developed normally u

231 re assayed for levels of estradiol, follicle-stimulating hormone, testosterone, and dehydroepiandrost

232 support the use of urinary or blood follicle-stimulating hormone tests or antimullerian hormone level

233 ulation of melanogenesis by alpha-melanocyte-stimulating hormone through melanocortin 1 receptor.

234 arkers of thyroid function including thyroid-stimulating hormone, thyroglobulin, total and free thyro

235 othyronine (T3) and thyroxine (T4)), thyroid-stimulating hormone, thyroid peroxidase antibodies, iodi

236 Ratios of follicle stimulating hormone to luteinizing hormone, a sexual mat

237 11 analytes included 9 hormones (ie, thyroid-stimulating hormone, total thyroxine, total triiodothyro

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

239 and competitive immunoassays, using thyroid stimulating hormone (TSH) and 17beta-estradiol (E2) as m

240 axis maintains circulating levels of thyroid stimulating hormone (TSH) and thyroid hormone (TH) in an

241 strate that GLIS3 acts downstream of thyroid-stimulating hormone (TSH) and TSH receptor (TSHR) and is

242 m, and is usually defined as a serum thyroid-stimulating hormone (TSH) concentration greater than the

243 Since thyroid-stimulating hormone (TSH) exerts an inductor effect on c

244 fication of pCB films with antihuman thyroid stimulating hormone (TSH) IgG molecules and the detectio

245 enocorticotropic hormone (ACTH), and thyroid stimulating hormone (TSH) in both normal and tumor tissu

246 he mediobasal hypothalamus (MBH) and thyroid-stimulating hormone (TSH) in the pituitary.

247 d free thyroxine (T4), total T4, and thyroid-stimulating hormone (TSH) in women during pregnancy, and

248 Semi-quantitative thyr oid stimulating hormone (TSH) lateral flow immunochromatogra

249 SCH was defined as a serum thyroid-stimulating hormone (TSH) level of 5.0 to 19.96 mIU/l wi

250 ata showing correlations between low thyroid-stimulating hormone (TSH) levels and high bone turnover

251 that exerts the hormonal control of thyroid-stimulating hormone (TSH) levels as well as neuromodulat

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

253 by low thyroid hormone (TH) and high thyroid-stimulating hormone (TSH) levels in the serum, is strong

254 collected, and thyroxine (T(4)) and thyroid-stimulating hormone (TSH) levels were measured at birth.

255 serum TH and inappropriately normal thyroid-stimulating hormone (TSH) levels, consistent with hypoth

256 positively associated with maternal thyroid-stimulating hormone (TSH) levels.

257 zed by high thyroid hormone (TH) and thyroid-stimulating hormone (TSH) levels.

258 ations for the functional reserve of thyroid-stimulating hormone (TSH) production and the TSH set poi

259 ice: 1) The development of the serum thyroid-stimulating hormone (TSH) radioimmunoassay led to the di

260 The thyroid-stimulating hormone (TSH) receptor signals via G(s) to p

261 g TH levels are tightly regulated by thyroid-stimulating hormone (TSH) secretion within the hypothala

262 tion rate was equivalent for the two thyroid-stimulating hormone (TSH) stimulation methods (thyroid h

263 hs; necropsy was performed and serum thyroid stimulating hormone (TSH) was measured.

264 It has long been known that thyroid stimulating hormone (TSH), a central component of the HP

265 rease in the pituitary expression of thyroid-stimulating hormone (TSH), an increase in the blood conc

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

267 ditis (AIT), serum concentrations of thyroid-stimulating hormone (TSH), and autoantibodies to thyrope

268 erum levels of free thyroxine (FT4), thyroid-stimulating hormone (TSH), and thyroid peroxidase antibo

269 that the anterior pituitary hormone, thyroid-stimulating hormone (TSH), can bypass the thyroid to exe

270 s according to genetically predicted thyroid stimulating hormone (TSH), free thyroxine (FT4) and thyr

271 s, including serum concentrations of thyroid-stimulating hormone (TSH), free thyroxine (FT4), and thy

272 total testosterone, prolactin (PRL), thyroid stimulating hormone (TSH), free triiodothyronine (fT3),

273 Serum levels of thyroid-stimulating hormone (TSH), total thyroxine (TT4), and PF

274 t depends on tanycyte sensitivity to thyroid stimulating hormone (TSH), which is dramatically and per

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

276 pharmaceuticals, negatively regulate thyroid-stimulating hormone (TSH)-dependent Ca(2+) increases and

277 Thyroid-stimulating hormone (TSH)-induced reduction in ligand bi

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

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

280 TC rapidly with high levels of serum thyroid-stimulating hormone (TSH).

281 l triiodothyronine (T3), free T4, or thyroid-stimulating hormone (TSH).

282 4) along with normalization of serum thyroid-stimulating hormone (TSH).

283 The thyrotropin [thyroid-stimulating hormone (TSH)] receptor (TSHR) is known to a

284 ence was presented that thyrotropin [thyroid-stimulating hormone (TSH)]-stimulated persistent cAMP si

285 ity and explore the relation between thyroid-stimulating hormone (TSH; also known as thyrotropin) lev

286 odimeric glycoprotein hormones, like thyroid-stimulating hormone (TSH; thyrotropin), have only recent

287 free triiodothyronine [TT3 and FT3], thyroid-stimulating hormone [TSH], and thyroglobulin [Tg]) and l

288 nt was POF, defined as at least one follicle-stimulating hormone value of > 40 IU/L after 2 years of

289 ine aminotransferase (p = 0.035) and thyroid-stimulating hormone values (p = 0.013) than those with n

290 78, 95% CI 2.00-16.67; p=0.001), and thyroid stimulating hormone was increased on average by 4.00 iU/

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

292 Thyroid-stimulating hormone was suppressed in patients given DIT

293 thyroxine </=10th percentile, normal thyroid-stimulating hormone) was associated with an increased od

294 e aromatase and the receptor of the follicle stimulating hormone were higher in contaminated fish tha

295 hyroxine, free triiodothyronine, and thyroid-stimulating hormone were measured in 1996 (n = 909) and

296 gesterone, luteinizing hormone, and follicle-stimulating hormone were measured in serum up to 8 times

297 gesterone, luteinizing hormone, and follicle-stimulating hormone were measured up to 8 times per cycl

298 one (GnRH) agonists and recombinant follicle-stimulating hormone were studied prospectively.

299 maintain high urine output; alpha-melanocyte-stimulating hormone, with anti-inflammatory and antiapop

300 r (DTC) may be prepared using either thyroid-stimulating hormone withdrawal (THW) or recombinant huma