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1 tion of the bone protein matrix (rickets and osteomalacia).
2 in vivo and in the etiology of drug-induced osteomalacia.
3 lates extracellularly, leading to rickets or osteomalacia.
4 t and C-terminal Fgf23 with hypophosphatemic osteomalacia.
5 an disease X-linked hypophosphatemic rickets/osteomalacia.
6 and low bone mineral density as a result of osteomalacia.
7 th a high risk of fragility fractures due to osteomalacia.
8 atemia, renal phosphate wasting, and rickets/osteomalacia.
9 taflox/y, and hyp-mice manifested comparable osteomalacia.
10 rum fibroblast growth factor-23 (Fgf23), and osteomalacia.
11 tion of 1,25-dihydroxyvitamin D, and rickets/osteomalacia.
12 ng a new molecular mechanism of drug-induced osteomalacia.
13 iating vitamin D catabolism and drug-induced osteomalacia.
14 nal effects of the hormone and contribute to osteomalacia.
15 malities, secondary hyperparathyroidism, and osteomalacia.
16 g adults and causes the painful bone disease osteomalacia.
17 7.08 microM [0.9-3.7 mg/dL]) and evidence of osteomalacia.
18 in the serum of a patient with tumor-induced osteomalacia.
19 to correct the hypophosphatemia, rickets, or osteomalacia.
20 with osteomalacia and 12 patients with focal osteomalacia.
21 of secondary hyperparathyroidism and severe osteomalacia.
22 phosphatase (TNSALP), results in rickets and osteomalacia.
23 ocalcemia, hyperparathyroidism, rickets, and osteomalacia.
24 he most common heritable form of rickets and osteomalacia.
25 itamin D levels, hypercalciuria, and rickets/osteomalacia.
26 secondary hyperparathyroidism, rickets, and osteomalacia, accompanied by 90% reduction in renal CaBP
27 87.5% of patients, including 9 patients with osteomalacia and 12 patients with focal osteomalacia.
28 milliliter in those with suspected oncogenic osteomalacia and 353+/-510 RU per milliliter (range, 31
32 ate kinase (PGK) promoter completely avoided osteomalacia and secondary hyperparathyroidism, and simu
33 er osteodystrophy characterized initially by osteomalacia and, more recently, by adynamic or aplastic
34 ophosphatemia, hyperparathyroidism, rickets, osteomalacia, and alopecia--the last a consequence of de
37 hypophosphatemia, characterized by rickets, osteomalacia, and hypomineralized dentin formation, a ph
38 low bone turnover, and generalized or focal osteomalacia are frequent histologic features in transpl
40 ) in mice, or its mutation in humans, causes osteomalacia believed to reflect renal phosphate wasting
41 5.4 +/- 0.1 mg/dl), and severity of rickets/osteomalacia (bone mineral density: -36, -36, and -30%).
42 mal serum calcidiol may avoid the problem of osteomalacia, but it does not correct malabsorption of c
44 nant hypophosphatemic rickets, and oncogenic osteomalacia demonstrate that elevated levels of novel c
47 lexural strength, and histologic evidence of osteomalacia; however, cultures of Hyp-derived bone marr
48 otypic changes, including dwarfism, rickets, osteomalacia, hypophosphatemia, increased serum parathyr
49 CasR deficiency, indicating that rickets and osteomalacia in CasR-deficient mice are not due to an in
50 s disorder are similar to those in oncogenic osteomalacia, in which tumors abundantly express FGF-23
55 5 years) and from 17 patients with oncogenic osteomalacia (mean age, 43.0+/-13.3 years) and 21 patien
59 ether it is elevated in those with oncogenic osteomalacia or X-linked hypophosphatemia, an immunometr
60 be markedly elevated in those with oncogenic osteomalacia or X-linked hypophosphatemia, suggesting th
63 al agent rifampin, resulting in drug-induced osteomalacia, which is attributed to vitamin D deficienc
64 pophosphatemic rickets, manifest rickets and osteomalacia with isolated renal phosphate-wasting assoc
65 content, expanded growth plates, and severe osteomalacia, with highly increased bone Fgf23 mRNA (>15
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