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1 ding severe cardiovascular disease and renal osteodystrophy.
2 d be used to improve the management of renal osteodystrophy.
3 ted the adynamic bone disorder form of renal osteodystrophy.
4 ous agent in treating animal models of renal osteodystrophy.
5 n of secondary hyperparathyroidism and renal osteodystrophy.
6 t of secondary hyperparathyroidism and renal osteodystrophy.
7 vating mutations lead to Albright hereditary osteodystrophy.
8 ack physical features of Albright hereditary osteodystrophy.
9 to ameliorate the skeletal lesions of renal osteodystrophy.
10 limited to PTH and lack Albright hereditary osteodystrophy.
11 somatic features termed Albright hereditary osteodystrophy.
12 the metabolic abnormalities that cause renal osteodystrophy.
13 t had no effect on vascular calcification or osteodystrophy.
14 tified in a patient with Albright hereditary osteodystrophy.
15 e implications for human Albright hereditary osteodystrophy, a condition caused by mutations in GNAS.
16 otopic ossification in Albright's hereditary osteodystrophy (AHO) and a recent report of two patients
18 tions lead to obesity in Albright hereditary osteodystrophy (AHO) patients, but only when the mutatio
24 pilepsy, and DOOR (deafness, onychdystrophy, osteodystrophy, and mental retardation) syndrome, and id
25 idney disease, vascular calcification, renal osteodystrophy, and phosphate contribute substantially t
26 imulated bone formation rates, corrected the osteodystrophy, and prevented CKD-stimulated vascular ca
27 rrected the hyperphosphatemia, corrected the osteodystrophy, and prevented VC, compatible with skelet
28 ith end-stage renal disease: a high-turnover osteodystrophy characterized by osteitis fibrosa, and a
29 ized by osteitis fibrosa, and a low-turnover osteodystrophy characterized initially by osteomalacia a
30 a, secondary hyperparathyroidism, and a mild osteodystrophy developed in the CKD/chow-fed group, as e
32 oid bone disease, the major variety of renal osteodystrophy, from developing in patients with renal i
33 premenopausal group, and patients with renal osteodystrophy had higher BW (41.4% +/- 9.6) than the pr
36 e DOORS syndrome: deafness, onychodystrophy, osteodystrophy, intellectual disability, and seizures.
40 latter analog, currently used to treat renal osteodystrophy, is more efficacious than 1,25(OH)2 D3 in
43 often acting on a background of preexisting osteodystrophy resulting from long-standing renal, hepat
44 Studies in patients with Albright hereditary osteodystrophy suggest a similar G(s)alpha imprinting pa
45 Uremic mice exhibited high turnover renal osteodystrophy; treatment with sevelamer significantly d
46 n its inception, CKD-MBD is characterized by osteodystrophy, vascular calcification, and stimulation
47 Superimposing CKD resulted in a low turnover osteodystrophy, whereas VC worsened and hyperphosphatemi
48 but without evidence for Albright hereditary osteodystrophy who has paternal uniparental isodisomy of
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