ライフサイエンスコーパス: parathyroid

1 tterning and organogenesis of the thymus and parathyroids.

2 Parathyroid 4-dimensional computed tomographic scans (4D

3 se To evaluate the diagnostic performance of parathyroid 4D CT and technetium 99m-sestamibi (hereafte

4 tiate between healthy parathyroid tissue and parathyroid adenoma from 18 patients.

5 ive reports, with pathologic confirmation of parathyroid adenoma or hyperplasia.

6 Moreover, the parathyroid adenoma subtypes (chief cells and oxyphil ce

7 (CDKN2A, CDKN2B and RASSF1A) was analysed in parathyroid adenoma tissues (n = 30).

8 alization procedure and imaging protocol for parathyroid adenoma.

9 can technique in the preoperative imaging of parathyroid adenoma.

10 Parathyroid adenomas and hyperplasia can be grouped into

11 14 in 94 patients with pathologically proven parathyroid adenomas or hyperplasia.

12 ectin-3 expression, consistent with atypical parathyroid adenomas, from 9 months of age.

13 1, a G1-S phase regulator, is upregulated in parathyroid adenomas.

14 tion-mediated inactivation of these genes in parathyroid adenomas.

15 lation of CCND1 regulatory genes in sporadic parathyroid adenomas.

16 here is little additional risk involved with parathyroid allotransplantation.

17 h Scandinavian Quality Register for Thyroid, Parathyroid and Adrenal Surgery and the Swedish National

18 h sensitivity-the unambiguous distinction of parathyroid and thyroid glands simultaneously in the con

19 None of the TPTX patients required delayed parathyroid AT to treat permanent hypoparathyroidism.

20 The rates of parathyroid autotransplantation (NTT 24% vs TT 28%, P =

21 ermanent hypoparathyroidism in patients with parathyroid autotransplantation [Odds ratio (OR) 1.72; 9

22 l thyroidectomy was high and associated with parathyroid autotransplantation, higher age, female sex

23 Preoperative parathyroid biopsy should be avoided.

24 and hyperplastic glands, and also in normal parathyroid by in situ hybridization, qRT-PCR, and immun

25 ribe the clinical presentation and workup of parathyroid carcinoma (PC) and determine its clinical pr

26 ial pHPT, reoperative parathyroidectomy, and parathyroid carcinoma are challenging entities that requ

27 lotting assays revealed that Sema3d inhibits parathyroid cell proliferation by decreasing the epiderm

28 binant Sema3d or derived peptides to inhibit parathyroid cell proliferation causing hyperplasia and h

29 Uremic rpS6(p-/-) mice had no increase in parathyroid cell proliferation compared with a marked in

30 mice with no increase in PTH mRNA levels and parathyroid cell proliferation compared with the 2- to 3

31 omplex 1 by rapamycin decreased or prevented parathyroid cell proliferation in secondary hyperparathy

32 e molecular pathways mediating the increased parathyroid cell proliferation remain undefined.

33 te that mTORC1 is a significant regulator of parathyroid cell proliferation through rpS6.

34 ed serum parathyroid hormone (PTH) level and parathyroid cell proliferation.

35 This activation correlated with increased parathyroid cell proliferation.

36 in PTH secretion from freshly-isolated human parathyroid cells consistent with a receptor-mediated ac

37 n modulate CaR responsiveness in HEK-293 and parathyroid cells independently of extracellular histidi

38 d active exogenous leptin uptake in cultured parathyroid cells.

39 n were detected in an overlapping fashion in parathyroid chief cells in adenoma and hyperplastic glan

40 sc confocal microscopy, electron microscopy, parathyroid culture, whole organ explant, and animal mod

41 rats and decreased levels of secreted PTH in parathyroid cultures.

42 The thymus and parathyroids develop from third pharyngeal pouch (3rd pp

43 encoding a transcription factor required for parathyroid development.

44 nvestigation and management of patients with parathyroid disorders.

45 was insufficient to expand the GCM2-positive parathyroid domain, indicating that multiple inputs, som

46 tigated the incidence of renal, thyroid, and parathyroid dysfunction in patients (aged >/=18 years) w

47 dependent of SHH signaling, are required for parathyroid fate specification.

48 Parathyroid four-dimensional (4D) CT has emerged as a pr

49 Parathyroids from uremic and normal rats segregated on t

50 ances may affect the CaR-mediated control of parathyroid function and calcium metabolism in vivo.

51 eed baseline measures of renal, thyroid, and parathyroid function and regular long-term monitoring.

52 arathyroidism indicates their importance for parathyroid function and the development of hyperparathy

53 Obtaining a parathyroid gland and a kidney from the same donor reduc

54 showed that this technique is able to detect parathyroid gland devascularization before it is visuall

55 not reverse the arrest in tooth, thymus, and parathyroid gland development, suggesting that the relat

56 was very low (3 mg/dl) due to damage to the parathyroid gland during total thyroidectomy for toxic g

57 glycoprotein, is expressed in the developing parathyroid gland in mice.

58 Surgical removal of hyperfunctional parathyroid gland is the definitive treatment for primar

59 UC) for localization of the hyperfunctioning parathyroid gland or glands at sestamibi SPECT/CT and 4D

60 arathyroidism can be cured by removal of the parathyroid gland or glands but identification of patien

61 he CaSR represents a phosphate sensor in the parathyroid gland, explaining the stimulatory effect of

62 rogenital tract, pancreas, liver, brain, and parathyroid gland.

63 The parathyroid glands acting through PTH play a critical ro

64 ptin is a functionally active product of the parathyroid glands and stimulates PTH release.

65 t EGFR signaling is elevated in Sema3d (-/-) parathyroid glands and that pharmacological inhibition o

66 ry conservation of abundant miRNAs in normal parathyroid glands and the regulation of these miRNAs in

67 scularized (n = 32) and compromised (n = 27) parathyroid glands during thyroid surgery with an accura

68 We profiled microRNA (miRNA) in parathyroid glands from experimental hyperparathyroidism

69 en early and late images of hyperfunctioning parathyroid glands in 44 patients (69%); in 13 patients

70 reoperative localization of hyperfunctioning parathyroid glands in a larger series of PHPT patients.

71 rathyroidism rats and in vitro in uremic rat parathyroid glands in organ culture.

72 on, with rates >fourfold higher than that in parathyroid glands of wild-type littermates (P<0.0001).

73 0.07) and the rate of inadvertently removed parathyroid glands was significantly higher after NTT (1

74 on: In most patients (89%), hyperfunctioning parathyroid glands were adequately visualized on early i

75 n), and had histologically proven pathologic parathyroid glands were retrospectively included in the

76 ur patients were included, and a total of 71 parathyroid glands were surgically removed.

77 receptor were present in normal and diseased parathyroid glands, and if so, whether they had any func

78 erations for bleeding, inadvertently removed parathyroid glands, and recurrent hyperthyroidism after

79 n vertebrate-specific tissues, placenta, and parathyroid glands, begging questions on the evolutionar

80 The same effect is seen in wild-type murine parathyroid glands, but not in CaSR knockout glands.

81 tiating single and multiple hyperfunctioning parathyroid glands, showed PET/CT to be most valuable in

82 dental disruption of blood supply to healthy parathyroid glands, which are responsible for regulating

83 requiring surgical removal of the offending parathyroid glands.

84 d hypercalcemia and caused by hypersecreting parathyroid glands.

85 n of the patients' hypoparathyroidism due to parathyroid graft rejection.

86 s identify Sema3d as a negative regulator of parathyroid growth.

87 splantation, persistent hyperparathyroidism (parathyroid hormone > 130 ng/L) and bone turnover marker

88 ge mean+/-SD single-pass renal extraction of parathyroid hormone (44.2%+/-10.3%) that exceeded the ex

89 Intermittent Parathyroid Hormone (I-PTH) is the only FDA approved ana

90 ients with hypercalcemia and elevated intact parathyroid hormone (iPTH) concentration were eligible i

91 nce interval (CI) 1.1-2.8], increasing serum parathyroid hormone (OR 1.1 per 10 pg/mL 95% CI 1.05-1.1

92 Intermittent administration of a fragment of Parathyroid hormone (PTH) activates osteoblast-mediated

93 Parathyroid hormone (PTH) activates receptors on osteocy

94 Parathyroid hormone (PTH) and calcium levels, recurrent

95 Parathyroid hormone (PTH) and FGF23 are the primary horm

96 a/c and levels of plasma phosphate, calcium, parathyroid hormone (PTH) and fibroblast growth factor 2

97 echanisms through which Pi intake stimulates parathyroid hormone (PTH) and fibroblast growth factor-2

98 coupled receptors (GPCRs) and natively binds parathyroid hormone (PTH) and parathyroid hormone relate

99 tissue development, has two native agonists, parathyroid hormone (PTH) and PTH-related protein (PTHrP

100 The bone catabolic actions of parathyroid hormone (PTH) are seen in patients with hype

101 Continuous parathyroid hormone (PTH) blocks its own osteogenic acti

102 ic whites, but whether adding information on parathyroid hormone (PTH) can help explain the higher ca

103 3 patients receiving hemodialysis with serum parathyroid hormone (PTH) concentrations higher than 500

104 ravenous calcimimetic etelcalcetide on serum parathyroid hormone (PTH) concentrations in patients rec

105 dc73(+/-) mice also had increased mean serum parathyroid hormone (PTH) concentrations.

106 Parathyroid hormone (PTH) has complex effects on bone, i

107 and urine levels of minerals, and levels of parathyroid hormone (PTH) in healthy postmenopausal wome

108 ide (PTHrP), prevented the decrease in serum Parathyroid Hormone (PTH) induced by lactation, but ampl

109 Genes related to the parathyroid hormone (PTH) influence cutaneous immune def

110 Parathyroid hormone (PTH) is a critical regulator of ske

111 Parathyroid hormone (PTH) is a primary calcium regulator

112 Parathyroid hormone (PTH) is an important regulator of o

113 Parathyroid hormone (PTH) is recognized to be an importa

114 Parathyroid hormone (PTH) is the only current anabolic t

115 yroidism is characterized by increased serum parathyroid hormone (PTH) level and parathyroid cell pro

116 ce and impact of HPT, defined as an elevated parathyroid hormone (PTH) level, after renal transplanta

117 ibited reduced serum inorganic phosphate and parathyroid hormone (PTH) levels and decreased bone form

118 Measuring the Parathyroid hormone (PTH) levels assists in the investig

119 ive agents 1,25(OH)(2)-vitamin D(3) (D3) and parathyroid hormone (PTH) on osteoclastogenesis.

120 otic-treated or germ-free mice, we show that parathyroid hormone (PTH) only caused bone loss in mice

121 Vitamin D and parathyroid hormone (PTH) regulate mineral metabolism an

122 aR) modulates renal calcium reabsorption and parathyroid hormone (PTH) secretion and is involved in t

123 ition of the abundant let-7 family increased parathyroid hormone (PTH) secretion in normal and uremic

124 , whether they had any functional effects on parathyroid hormone (PTH) secretion in parathyroid neopl

125 Intermittent administration of parathyroid hormone (PTH) stimulates bone formation in v

126 Upon parathyroid hormone (PTH) stimulation, the PTHR internal

127 Circulating parathyroid hormone (PTH), 25(OH)D, calcium and peripher

128 In response to parathyroid hormone (PTH), a bone anabolic hormone, LepR

129 Human parathyroid hormone (PTH), a member of class B GPCRs, bi

130 Serum parathyroid hormone (PTH), calcium, phosphorus and alkal

131 BD) parameters including calcium, phosphate, parathyroid hormone (PTH), fibroblast growth factor 23 (

132 y regulated in a highly reciprocal manner by parathyroid hormone (PTH), fibroblast growth factor 23 (

133 mber 1 (CYP27B1), whose gene is regulated by parathyroid hormone (PTH), fibroblast growth factor 23 (

134 ercalcemic patients underwent measurement of parathyroid hormone (PTH), had documentation of hypercal

135 Teriparatide, a recombinant form of parathyroid hormone (PTH), is the only approved treatmen

136 transferrin saturation (TSAT) concentration, parathyroid hormone (PTH), IV vitamin D dose, cinacalcet

137 ata defined by their pretransplant levels of parathyroid hormone (PTH), low PTH (>65 to </=300 pg/mL;

138 ced bone deposition with decreased levels of parathyroid hormone (PTH), which is a key regulator of b

139 des: glucagon-like peptide-1 (GLP-1) and the parathyroid hormone (PTH), which respectively help contr

140 al to Cyp27b1 that mediates unique basal and parathyroid hormone (PTH)-, fibroblast growth factor 23

141 m MS analysis, we characterized the sites of parathyroid hormone (PTH)-induced NHERF1 phosphorylation

142 m baseline in blood and urine markers of the parathyroid hormone (PTH)-vitamin D-fibroblast growth fa

143 st growth factor 23 (FGF23) and reduction of parathyroid hormone (PTH).

144 iciting concentration-dependent secretion of parathyroid hormone (PTH).

145 ostasis and is tightly regulated through the parathyroid hormone (PTH)/PTHrP receptor (PTH1R) signali

146 We reveal the existence of an ancient parathyroid hormone (Pth)4 in zebrafish that was seconda

147 Parathyroid hormone (PTH, 84 residues) and PTH-related p

148 The parathyroid hormone 1 receptor (PTHR) is central to the

149 In another study, we showed that parathyroid hormone 1-34 and anti-sclerostin antibody at

150 Studies by Sato et al. reveal a role for parathyroid hormone 2 receptor (PTH2R) in extracellular

151 f 39 residues (TIP39), via its receptor, the parathyroid hormone 2 receptor (PTH2R), modulates fear m

152 Small interfering RNA-mediated silencing of parathyroid hormone 2 receptor (PTH2R), the receptor for

153 Synthetic parathyroid hormone [PTH(1-34)] has been investigated fo

154 signature of the arrestin pathway-selective parathyroid hormone analog [d-Trp(12), Tyr(34)]bovine PT

155 splant patients significantly reduced intact parathyroid hormone and increased fibroblast growth fact

156 P(i) and various hormones, including parathyroid hormone and phosphatonins, such as fibroblas

157 ts of histologic analysis, as well as intact parathyroid hormone and serum calcium values obtained 1

158 Paricalcitol decreases intact parathyroid hormone and the frequency of secondary hyper

159 alphas also inhibited internalization of the parathyroid hormone and type 2 vasopressin receptors.

160 terminal propeptide (PINP), osteocalcin, and parathyroid hormone as well as a transient decrease in t

161 substantial single-pass renal extraction of parathyroid hormone at a rate that exceeds glomerular fi

162 hly expressed in osteocytes, is regulated by parathyroid hormone both in vitro and in vivo, and prote

163 nine, lower hematocrit, and increased intact parathyroid hormone but did not demonstrate any differen

164 However, parathyroid hormone concentrations decreased in all 3 gr

165 The proportionate renal extraction of parathyroid hormone correlated with eGFR.

166 Intact parathyroid hormone decreased in paricalcitol-treated pa

167 a common endocrine disease characterized by parathyroid hormone excess and hypercalcemia and caused

168 with decreased creatinine, phosphorous, and parathyroid hormone in the rats with CKD.

169 ium concentration is within normal range but parathyroid hormone is elevated in the absence of any ob

170 x, and creatinine clearance, but with intact parathyroid hormone less than 100 pg/mL, were included a

171 rogression were age, baseline total or whole parathyroid hormone level greater than nine times the no

172 Regarding modifiable factors, higher average parathyroid hormone level was associated with greater ri

173 walking, and higher average log-transformed parathyroid hormone level were independently associated

174 sphatemia and hypomagnesemia with low plasma parathyroid hormone level.

175 Patients on HD with intact parathyroid hormone levels </=300 pg/ml receiving dialys

176 nover in patients on HD with baseline intact parathyroid hormone levels </=300 pg/ml.

177 lerated) or nonparicalcitol therapy on serum parathyroid hormone levels (primary outcome), mineral me

178 s induced by aldosteronism in which elevated parathyroid hormone levels raise the risk of adverse car

179 Median intact parathyroid hormone levels were lower and severe hyperpa

180 mice had significantly lower serum FGF23 and parathyroid hormone levels, and higher renal 1-alpha-hyd

181 In this study, we report that TIP39, a parathyroid hormone ligand family member that was recent

182 Pth4, an ancient parathyroid hormone lost in eutherian mammals, reveals a

183 Impaired renal clearance of parathyroid hormone may contribute to secondary hyperpar

184 y invasive parathyroidectomy, intraoperative parathyroid hormone monitoring via a reliable protocol i

185 olysis contribute to the anabolic actions of parathyroid hormone on the skeleton.

186 strogen deficiency and sustained exposure to parathyroid hormone or RANKL.

187 The G protein-coupled parathyroid hormone receptor (PTHR) regulates mineral-io

188 The type-1 parathyroid hormone receptor (PTHR1), which regulates ca

189 Parathyroid hormone receptor 1 (PTH1R) belongs to the se

190 The parathyroid hormone receptor 1 (PTHR1) is a member of th

191 The parathyroid hormone receptor-1 (PTH1R) is a class B G pr

192 We address activation of parathyroid hormone receptor-1 (PTHR1) and improve the s

193 tain interacting partners such as Lfc or the parathyroid hormone receptor.

194 , Ctsk deletion in osteocytes increased bone Parathyroid Hormone related Peptide (PTHrP), prevented t

195 natively binds parathyroid hormone (PTH) and parathyroid hormone related peptide (PTHrP).

196 nthracenyl-terpyridine as a modulator of the parathyroid hormone response.

197 ices with isoproterenol, norepinephrine, and parathyroid hormone similarly increased NCC phosphorylat

198 Osteo-active parathyroid hormone treatment abolishes infection-trigge

199 Serum albumin, 25(OH)D, and intact parathyroid hormone were measured.

200 actor 23 was, on average, lower than that of parathyroid hormone with greater variability across indi

201 5-hydroxyvitamin D, phosphorus, calcium, and parathyroid hormone).

202 racteristics, dietary intakes, fasting serum parathyroid hormone, 25-hydroxyvitamin D [25(OH)D], and

203 ium, phosphorus, 25-hydroxyvitamin D, intact parathyroid hormone, and 24,25-dihydroxyvitamin D did no

204 use of monoclonal or polyclonal antibodies), parathyroid hormone, and albumin.

205 he HDF cohort had lower beta2-microglobulin, parathyroid hormone, and high-sensitivity C-reactive pro

206 ar, serum osteocalcin, total calcium, intact parathyroid hormone, and increased serum C telopeptide.

207 , creatinine clearance, phosphorus, calcium, parathyroid hormone, and no cortical porosity).

208 plasma levels of FGF23, calcium, phosphate, parathyroid hormone, and vitamin D metabolites.

209 FGF23, despite having high concentrations of parathyroid hormone, but administration of exogenous 1,2

210 evels, serum calcium homeostasis biomarkers (parathyroid hormone, calcium, and 25-hydroxyvitamin D),

211 minal aortic calcification, serum phosphate, parathyroid hormone, FGF23, and 24-hour urinary phosphat

212 etermined the single-pass renal clearance of parathyroid hormone, fibroblast growth factor 23, vitami

213 ccurred in serum calcium, phosphorus, intact parathyroid hormone, or C-reactive protein levels, cinac

214 not be explained by hypocalcemia, changes in parathyroid hormone, or fibroblast growth factor 23.

215 etabolic pathway (e.g., 25-hydroxyvitamin D, parathyroid hormone, phosphorus) had little impact.

216 nine, free thyroxine, free triiodothyronine, parathyroid hormone, prolactin, N-terminal pro-brain nat

217 as phosphates, fibroblast growth factor 23, parathyroid hormone, sclerostin, or vitamin D and their

218 Beyond hypophosphatemia and increased parathyroid hormone, the most common adverse drug reacti

219 me BP, plasma and urine electrolytes, renin, parathyroid hormone, vitamin D, and response to oral glu

220 More biochemical surveillance particularly a parathyroid hormone-based protocol, fine-tuned supplemen

221 der these circumstances both agents enhanced parathyroid hormone-induced osteoblast differentiation a

222 coid receptor to potentiate vitamin D(3) and parathyroid hormone-induced osteoclastogenesis.

223 , and Ihh target genes Patched 1 (Ptch1) and parathyroid hormone-like peptide (Pthlh) were down-regul

224 The majority of cells expressing parathyroid hormone-related peptide (PTHrP) are in the d

225 Parathyroid hormone-related peptide (PTHrP) is recognize

226 pression in chondrocytes strictly depends on parathyroid hormone-related peptide (PTHrP) signaling pa

227 r translocation of Gli2 and transcription of parathyroid hormone-related peptide (PTHrP), a key regul

228 st and prostate cancer metastasis biomarker, parathyroid hormone-related peptide (PTHrP).

229 ATDC5 chondrogenic cells is downregulated by parathyroid hormone-related peptide through transcriptio

230 ix protein 1, a direct targeting molecule of parathyroid hormone-related peptide, negatively regulate

231 ells are regulated by autocrine signaling by parathyroid hormone-related protein (PTHrP) and its para

232 Parathyroid hormone-related protein (PTHrP) contributes

233 K14-PTHrP transgenic mice [which overexpress parathyroid hormone-related protein (PTHrP) in their dev

234 Parathyroid hormone-related protein (PTHrP) is a critica

235 nscription factor Gli2 as a key regulator of parathyroid hormone-related protein (PTHrP), which is pr

236 sion data suggested that the Indian Hedgehog-parathyroid hormone-related protein signaling axis was i

237 as been made in determining the roles of the parathyroid hormone-related protein, Indian hedgehog, fi

238 er characterized by autonomous production of parathyroid hormone.

239 or inappropriately normal concentrations of parathyroid hormone.

240 ts increase is associated with a decrease in parathyroid hormone.

241 (receptor activator of NFkappaB ligand) and parathyroid hormone.

242 clic AMP responded to external cues, such as parathyroid hormone.

243 hyroid tissue causing excessive secretion of parathyroid hormone.

244 ized by hypercalcemia and elevated levels of parathyroid hormone.

245 roid hormone-related protein (PTHrP) and its parathyroid hormone/PTHrP receptor PPR.

246 er levels of serum calcium, phosphorous, and parathyroid hormone; and nutritional vitamin D, cinacalc

247 The PTH1R (PTH [parathyroid hormone]/PTHrP [PTH-related protein] recepto

248 Parathyroid-hormone-type 1 receptor (PTH1R) is extensive

249 two-session radiofrequency ablation (RFA) of parathyroid hyperplasia for patients with secondary hype

250 US-guided RFA of parathyroid hyperplasia is a safe and effective method f

251 n of EGFR signaling can partially rescue the parathyroid hyperplasia phenotype.

252 ved that genetic deletion of Sema3d leads to parathyroid hyperplasia, causing PHPT.

253 hyroidism underwent ultrasound guided RFA of parathyroid hyperplasia.

254 the acquisition of dual-time-point images in parathyroid imaging with (18)F-FCH PET/CT or the creatio

255 id nodule (OR, 1.82; 95% CI, 1.01-3.28), and parathyroid lesion in the inferior position (OR, 6.82; 9

256 CTs and intraoperative findings, followed by parathyroid lesion in the inferior position and parathyr

257 Parathyroid lesion size of 10 mm or less (odds ratio [OR

258 athyroid lesion in the inferior position and parathyroid lesion size of 10 mm or less.

259 characterize factors associated with missed parathyroid lesions on preoperative 4D-CTs and to invest

260 dings in the number and location of abnormal parathyroid lesions.

261 We identified parathyroid miRNAs that were dysregulated in experimenta

262 Using the following key terms: "parathyroid, near infrared, autofluorescence" in various

263 ts on parathyroid hormone (PTH) secretion in parathyroid neoplasms.

264 e yet considerably limited in complexity (no parathyroids, no skin).

265 d that the mTOR pathway was activated in the parathyroid of rats with secondary hyperparathyroidism i

266 normal and uremic rats, as well as in mouse parathyroid organ cultures.

267 activity of GCM2, suggesting that GCM2 is a parathyroid proto-oncogene.

268 recurrent or persistent hyperparathyroidism, parathyroid reoperations, morbidity, and mortality were

269 id transplantation may represent a permanent parathyroid replacement therapy.

270 rm a technetium 99m sestamibi ((99m)Tc MIBI) parathyroid scan.

271 deep-sequencing showed that human and rodent parathyroids share similar profiles.

272 ed conventional (Cdc73(+/-)) and conditional parathyroid-specific (Cdc73(+/L)/PTH-Cre and Cdc73(L/L)/

273 ommendations for patients who do not undergo parathyroid surgery include monitoring of serum calcium

274 ding which patients should be considered for parathyroid surgery.

275 py was used to differentiate between healthy parathyroid tissue and parathyroid adenoma from 18 patie

276 mary cause of PHPT is a benign overgrowth of parathyroid tissue causing excessive secretion of parath

277 athyroidism is due to a benign overgrowth of parathyroid tissue either as a single gland (80% of case

278 plantation of allogeneic thymus and parental parathyroid tissue has been attempted but does not achie

279 ization confirmed the presence of allogeneic parathyroid tissue in the patient's thymus transplant bi

280 ed parathyroid tissue may be used to confirm parathyroid tissue intraoperatively.

281 It is recognised that ectopic parathyroid tissue is not infrequently found in the thym

282 Ex vivo aspiration of resected parathyroid tissue may be used to confirm parathyroid ti

283 Devascularized normal parathyroid tissue should be autotransplanted.

284 ilt to discriminate healthy from adenomatous parathyroid tissue was able to correctly classify all sa

285 0 mg of adenomatous or hyperplastic diseased parathyroid tissue was prepared and processed according

286 lation of these genes was observed in normal parathyroid tissue.

287 (p < 0.01) in adenomatous compared to normal parathyroid tissue.

288 Parathyroid transplantation may represent a permanent pa

289 lated cell cycle mechanism may contribute to parathyroid tumorigenesis.

290 Parathyroid tumour development, and elevations in serum

291 ies, which have established mouse models for parathyroid tumours and uterine neoplasms that develop i

292 Parathyroid tumours in Cdc73(+/-), Cdc73(+/L)/PTH-Cre an

293 nant disorder characterized by occurrence of parathyroid tumours, often atypical adenomas and carcino

294 TH-Cre and Cdc73(L/L)/PTH-Cre mice developed parathyroid tumours, which had nuclear pleomorphism, fib

295 dized uptake value (SUVmax) between abnormal parathyroid uptake and physiologic thyroid uptake.

296 y images showed a decrease over time in both parathyroid uptake and the ratio of parathyroid uptake t

297 e was a significant increase in the ratio of parathyroid uptake to thyroid uptake (P = 0.037).

298 erences in (18)F-FCH uptake and the ratio of parathyroid uptake to thyroid uptake between the latter

299 in both parathyroid uptake and the ratio of parathyroid uptake to thyroid uptake, significant in com

300 t Imaging (LSCI) for real-time assessment of parathyroid viability.