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1 rogenital tract, pancreas, liver, brain, and parathyroid gland.
2 thymus hypoplasia and mislocalization of the parathyroid gland.
3 requiring surgical removal of the offending parathyroid glands.
4 ur parathyroid glands and resecting enlarged parathyroid glands.
5 best tool available for imaging of abnormal parathyroid glands.
6 ion of calcium homeostasis in the absence of parathyroid glands.
7 factor whose expression is restricted to the parathyroid glands.
8 cule exists in zebrafish, species which lack parathyroid glands.
9 ction that is expressed in the pituitary and parathyroid glands.
10 thyroid glands in one patient, and 51 normal parathyroid glands.
11 aging device was used to image a total of 37 parathyroid glands.
12 order caused by one or more hyperfunctioning parathyroid glands.
13 cell microenvironment in both human and NHP parathyroid glands.
14 detect similar differences in blood flow to parathyroid glands.
15 d hypercalcemia and caused by hypersecreting parathyroid glands.
16 he likelihood of additional hyperfunctioning parathyroid glands.
17 ized by precise preoperative localization of parathyroid glands.
18 , the coreceptor for FGF23 in the kidney and parathyroid glands.
19 retion of parathyroid hormone (PTH) from the parathyroid glands.
20 continue to guide surgical resection of the parathyroid glands.
21 ng endodermal progenitors of both thymus and parathyroid glands.
22 CD44/CD24 population was 10.93% for enlarged parathyroid glands.
23 by varying defects of the heart, thymus, and parathyroid glands.
24 rathyroid imaging except in locating ectopic parathyroid glands.
25 ied 89% of the surgically confirmed diseased parathyroid glands.
26 metabolism and a potent hormone made by the parathyroid glands.
27 ide counts > background to localize abnormal parathyroid glands.
29 c-sestamibi scan demonstrated a hyperplastic parathyroid gland, a large anterior mediastinal mass and
31 o vitamin D2-treated animals with suppressed parathyroid gland activity produced marked elevation in
32 regulate overactivity and hyperplasia of the parathyroid gland after the onset of renal insufficiency
34 uorescence intensity was calculated for each parathyroid gland and compared with speckle contrast in
35 receptor proteins (CaRs) enable cells in the parathyroid gland and kidney thick ascending limb of Hen
37 ardiac outflow defects and hypoplasia of the parathyroid gland and thymus due to haploinsufficiency o
38 g CD44 antibody was performed on 27 abnormal parathyroid glands and 7 normal parathyroid gland biopsi
39 ent mice in association with ablation of the parathyroid glands and correction of the severe hyperpar
41 Here we show that Gcm2-deficient mice lack parathyroid glands and exhibit a biological hypoparathyr
42 the white matter of uremic dogs with intact parathyroid glands and in normal dogs and TPTX uremic do
43 binding protein-beta, in human hyperplastic parathyroid glands and in the human epidermoid carcinoma
44 roidism is due to enlargement of one or more parathyroid glands and is most often treated by surgical
45 he likelihood of additional hyperfunctioning parathyroid glands and let the surgeon determine whether
46 1(-/-) double knockout mice preserved intact parathyroid glands and reinstated CKD-induced secondary
47 eleton, we used a genetic approach to ablate parathyroid glands and remove the confounding effects of
48 the neck with the intent of visualizing four parathyroid glands and resecting enlarged parathyroid gl
50 t EGFR signaling is elevated in Sema3d (-/-) parathyroid glands and that pharmacological inhibition o
51 ry conservation of abundant miRNAs in normal parathyroid glands and the regulation of these miRNAs in
52 n aging-related protein found in the kidney, parathyroid gland, and choroid plexus, acts as an essent
54 n protein predominantly expressed in kidney, parathyroid glands, and choroids plexus of the brain.
55 receptor were present in normal and diseased parathyroid glands, and if so, whether they had any func
56 erations for bleeding, inadvertently removed parathyroid glands, and recurrent hyperthyroidism after
57 rior lobes of the pituitary, the thyroid and parathyroid glands, and the adrenal medulla within the f
59 al pharyngeal pouch derivatives (the thymus, parathyroid glands, and thyroid gland), heart, and gut.
65 ccompanied by an increase in the size of the parathyroid gland as well as an increase in PTH mRNA lev
66 the effects of extracellular calcium in the parathyroid gland as well as other tissues has been iden
68 n vertebrate-specific tissues, placenta, and parathyroid glands, begging questions on the evolutionar
70 tivating the calcium-sensing receptor in the parathyroid glands, but clinical experience with them is
74 imaging modality in localizing pathological parathyroid glands, calculated on a per-quadrant and a p
75 elated to the accuracy of localizing ectopic parathyroid glands, calls for a refinement of interpreta
76 ures, including hypoplasia of the thymus and parathyroid glands, cardiac outflow tract abnormalities,
77 Altered CaSR expression in the kidney or the parathyroid glands could not account for the observed ph
78 m (PHPT), discovering a minimally "enlarged" parathyroid gland creates a dilemma for the surgeon rega
79 nd laser confocal microscopy of normal human parathyroid gland demonstrated expression of parafibromi
80 tions of the aortic arch, heart, thymus, and parathyroid glands described as DiGeorge syndrome (DGS).
81 showed that this technique is able to detect parathyroid gland devascularization before it is visuall
83 not reverse the arrest in tooth, thymus, and parathyroid gland development, suggesting that the relat
86 was very low (3 mg/dl) due to damage to the parathyroid gland during total thyroidectomy for toxic g
89 scularized (n = 32) and compromised (n = 27) parathyroid glands during thyroid surgery with an accura
90 yroidism is due to increased activity of the parathyroid glands, either from an intrinsic abnormal ch
91 of function of the GCMB gene impairs normal parathyroid gland embryology and is responsible for isol
92 cterized primarily by multiple tumors in the parathyroid glands, endocrine pancreas, and anterior pit
95 he CaSR represents a phosphate sensor in the parathyroid gland, explaining the stimulatory effect of
96 PT may result from reduced expression of the parathyroid gland extracellular Ca(2+)-sensing receptor
97 ne-associated antigen of 120-140 kD in human parathyroid gland extracts using immunoblot analysis.
100 obtained for FACS analysis from 25 enlarged parathyroid glands from 20 patients, 17 with primary HPT
103 ivation analyses have demonstrated that most parathyroid glands from patients with uremic refractory
107 n bone mineralization, vitamin D metabolism, parathyroid gland function, and renal phosphate handling
109 , intravenous calcitriol appears to decrease parathyroid gland functional mass, as reflected by decre
111 Radioguided resection of hyperfunctioning parathyroid glands has been shown to be technically feas
113 l phenotype, which were manifested by larger parathyroid glands, higher serum parathyroid hormone lev
114 djunctive intraoperative tool for localizing parathyroid glands; however, its potential utility in th
115 of hypoPT has involved visual inspection of parathyroid glands; however, near-infrared autofluoresce
117 maps of the chromatin landscape of the human parathyroid glands, identifying active regulatory elemen
118 lume group were more likely to have a missed parathyroid gland in a normal anatomic location (89% vs.
120 se, Met-PET/CT identified 2 hyperfunctioning parathyroid glands in 1 patient, 1 gland in 3 individual
122 en early and late images of hyperfunctioning parathyroid glands in 44 patients (69%); in 13 patients
123 reoperative localization of hyperfunctioning parathyroid glands in a larger series of PHPT patients.
124 cular imaging for localizing visually occult parathyroid glands in both anatomic and ectopic location
125 PET/CT for localization of hyperfunctioning parathyroid glands in comparison with other imaging test
126 in SHP, increased PTH expression ex vivo in parathyroid glands in culture and in transfected cells t
127 ative failure can be due to hyperfunctioning parathyroid glands in ectopic locations, less experience
130 adenomas in one patient; and 3 hyperplastic parathyroid glands in one patient, and 51 normal parathy
132 ferred method for detecting hyperfunctioning parathyroid glands in patients with clinical hyperparath
133 th SPECT/CT for the localization of abnormal parathyroid glands in patients with primary hyperparathy
137 nt this complication include preservation of parathyroid glands in situ and autotransplantation of pa
139 e thyroidectomies attempting to preserve the parathyroid glands in situ with an intact vascular pedic
141 ion computed tomography to localize enlarged parathyroid glands in three dimensions, limited explorat
145 d and is essential for maintaining postnatal parathyroid gland integrity throughout life and for the
146 t the secretion of PTH by chief cells in the parathyroid gland is regulated by extracellular ionized
148 ing receptor (CaSR), first identified in the parathyroid gland, is expressed in several tissues and c
149 autonomous growth in two, three, or all four parathyroid glands, is a distinct molecular entity and d
151 wed specific immunoreactivity in adrenal and parathyroid glands, kidney, heart, and skeletal muscle.
152 emic level causes promiscuous effects in the parathyroid glands, kidneys, and other tissues, and the
153 rain regions, coronary arteries, thyroid and parathyroid glands, large intestine, colon, bladder, tes
154 n the general population, blacks have higher parathyroid gland mass and circulating parathyroid hormo
155 s known to be required for normal thymus and parathyroid gland morphogenesis, whereas Pax1, Hoxa3, Ey
156 ostic study analyzed in vivo NIRAF images of parathyroid glands obtained during parathyroidectomies b
157 show that loss of Men1 gene function in the parathyroid glands of mice results in histological chang
158 on, with rates >fourfold higher than that in parathyroid glands of wild-type littermates (P<0.0001).
159 secondary outcome was the visibility of each parathyroid gland on NIRAF imaging before it became appa
160 tigraphy separately showed a hyperfunctional parathyroid gland on the same side or in the same ectopi
161 UC) for localization of the hyperfunctioning parathyroid gland or glands at sestamibi SPECT/CT and 4D
162 arathyroidism can be cured by removal of the parathyroid gland or glands but identification of patien
164 e brain, musculoskeletal system, thyroid and parathyroid glands, pancreas, kidney, lung, and breast;
165 Despite the sustained stimulation to the parathyroid gland, parathyroid cells did not undergo hyp
166 -/-) mice displayed apoptotic loss of intact parathyroid glands postnatally and reduced mechanistic t
167 cts of dietary P on serum PTH, PTH mRNA, and parathyroid gland (PTG) hyperplasia in uremic rats.
168 Accurate identification and preservation of parathyroid glands (PTG) during thyroidectomy are crucia
169 urce for unraveling the mechanisms governing parathyroid gland regulation in health and disease.
171 iple Endocrine Neoplasia type 2A should have parathyroid glands resected at the time of thyroidectomy
173 id glands in situ and autotransplantation of parathyroid glands resected or devascularized during thy
174 d by hypoplasia or atresia of the thymus and parathyroid glands resulting in T cell-mediated deficien
175 racellular calcium ions (Ca2+o), cloned from parathyroid gland, serves a critical function in Ca2+o h
176 tiating single and multiple hyperfunctioning parathyroid glands, showed PET/CT to be most valuable in
178 hyroidism and enlargement of only one or two parathyroid glands that the resection be limited to thes
179 This axis is essential for preserving intact parathyroid glands throughout life, with relevance to CK
180 , but does not affect the sensitivity of the parathyroid gland to changes in iCa, as set point and no
181 ]o) in the physiological range, allowing the parathyroid gland to regulate serum [Ca2+]o; however, th
182 within the physiological range, allowing the parathyroid gland to regulate serum Ca(o); however, the
183 The accuracy for localizing a pathologic parathyroid gland to the correct side of the neck was 59
186 0.07) and the rate of inadvertently removed parathyroid glands was significantly higher after NTT (1
187 upled receptor for external Ca2+ cloned from parathyroid gland, was shown to be expressed in PF cells
188 cytometric analysis of resected adenomatous parathyroid glands, we have isolated and characterized c
189 am, consisting of the combination of WIN and parathyroid gland weight, accurately predicted the likel
190 xcision, radionuclide counts of each ex vivo parathyroid gland were determined and expressed as a per
191 on: In most patients (89%), hyperfunctioning parathyroid glands were adequately visualized on early i
197 s 61% [95% CI, 56%-66%]) (P < .001) and less parathyroid glands were inadvertently excised (4% [95% C
199 n), and had histologically proven pathologic parathyroid glands were retrospectively included in the
201 dental disruption of blood supply to healthy parathyroid glands, which are responsible for regulating
202 mic progression of cell states within normal parathyroid glands, which can be used to better understa
203 ts from the calcium-sensing receptors on the parathyroid glands, which detect changes in calcium conc
204 arathyroid adenomas are benign tumors in the parathyroid glands, whose pathogenesis is largely unknow