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1 defects were present in human patients with hypophosphatemic rickets.
2 he periodontal status of adult patients with hypophosphatemic rickets.
3 keletal abnormalities in two mouse models of hypophosphatemic rickets.
4 ved in the Dmp1 null mouse, a mouse model of hypophosphatemic rickets.
5 very of a novel disease: autosomal-recessive hypophosphatemic rickets.
6 factor 23 (FGF-23) cause autosomal dominant hypophosphatemic rickets.
7 in individuals receiving medical therapy for hypophosphatemic rickets.
8 sociated with the autosomal dominant form of hypophosphatemic rickets.
9 ed, had dentin and enamel defects as well as hypophosphatemic rickets.
10 ization pattern characteristic for dentin in hypophosphatemic rickets.
11 tein 1 (DMP-1) result in increased FGF23 and hypophosphatemic rickets.
12 , and was ultimately diagnosed with X-linked hypophosphatemic rickets, a disorder caused by renal was
16 The metabolic disorder autosomal dominant hypophosphatemic rickets (ADHR) was previously mapped to
18 periodontal condition of adults with genetic hypophosphatemic rickets and compared their periodontal
19 sis/hyperostosis hyperphosphatemia syndrome, hypophosphatemic rickets, and hypophosphatasia), and bon
20 hypophosphatemic rickets, autosomal-dominant hypophosphatemic rickets, and oncogenic osteomalacia dem
21 ice, the murine homolog of X-linked dominant hypophosphatemic rickets, and transgenic mice that overe
22 in matrix protein 1-null mice, which are the hypophosphatemic rickets animal model, postnatally devel
23 a from our study suggests that patients with hypophosphatemic rickets are more prone to periodontal b
25 novel mechanism of phosphaturia in X-linked hypophosphatemic rickets, autosomal-dominant hypophospha
26 altered phosphate metabolism and symptoms of hypophosphatemic rickets, circling behavior, hyperactivi
28 nal analyses showed that autosomal recessive hypophosphatemic rickets family carried a mutation affec
31 factor in the pathogenesis of rare forms of hypophosphatemic rickets is rapidly reshaping our unders
33 wly identified disorder, autosomal recessive hypophosphatemic rickets, manifest rickets and osteomala
34 tivity in the pathogenesis of FGF23-mediated hypophosphatemic rickets, more work will need to be done
36 Additionally, Xpr1-deficient mice developed hypophosphatemic rickets secondary to renal dysfunction.
38 20C conditional knock-out (KO) mice manifest hypophosphatemic rickets, which highlights the crucial r
41 e cotransporter 2c (NPT2c), cause hereditary hypophosphatemic rickets with hypercalciuria (HHRH), a d
42 n infancy and the treatment of patients with hypophosphatemic rickets with phosphate and vitamin D pr
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