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1 e X-linked hypophosphatemia (XLH), a form of hypophosphatemic rickets.
2 ization pattern characteristic for dentin in hypophosphatemic rickets.
3 tein 1 (DMP-1) result in increased FGF23 and hypophosphatemic rickets.
4  defects were present in human patients with hypophosphatemic rickets.
5 he periodontal status of adult patients with hypophosphatemic rickets.
6 ved in the Dmp1 null mouse, a mouse model of hypophosphatemic rickets.
7 very of a novel disease: autosomal-recessive hypophosphatemic rickets.
8  factor 23 (FGF-23) cause autosomal dominant hypophosphatemic rickets.
9 in individuals receiving medical therapy for hypophosphatemic rickets.
10 keletal abnormalities in two mouse models of hypophosphatemic rickets.
11 blast growth factor 23 (FGF23) in hereditary hypophosphatemic rickets.
12 sociated with the autosomal dominant form of hypophosphatemic rickets.
13 ed, had dentin and enamel defects as well as hypophosphatemic rickets.
14 , and was ultimately diagnosed with X-linked hypophosphatemic rickets, a disorder caused by renal was
15                                     X-linked hypophosphatemic rickets, a dominantly inherited disease
16                           Autosomal dominant hypophosphatemic rickets (ADHR) is an inherited disorder
17                           Autosomal dominant hypophosphatemic rickets (ADHR) is unique among the diso
18    The metabolic disorder autosomal dominant hypophosphatemic rickets (ADHR) was previously mapped to
19       In the Hyp-mouse homologue of X-linked hypophosphatemic rickets, administration of 1,25(OH)(2)D
20 periodontal condition of adults with genetic hypophosphatemic rickets and compared their periodontal
21 sis/hyperostosis hyperphosphatemia syndrome, hypophosphatemic rickets, and hypophosphatasia), and bon
22 hypophosphatemic rickets, autosomal-dominant hypophosphatemic rickets, and oncogenic osteomalacia dem
23 ice, the murine homolog of X-linked dominant hypophosphatemic rickets, and transgenic mice that overe
24 in matrix protein 1-null mice, which are the hypophosphatemic rickets animal model, postnatally devel
25 a from our study suggests that patients with hypophosphatemic rickets are more prone to periodontal b
26 cise mechanisms of how excess FGF23 leads to hypophosphatemic rickets are not clear.
27  novel mechanism of phosphaturia in X-linked hypophosphatemic rickets, autosomal-dominant hypophospha
28 altered phosphate metabolism and symptoms of hypophosphatemic rickets, circling behavior, hyperactivi
29                           An adolescent with hypophosphatemic rickets developed cardiac calcification
30 nal analyses showed that autosomal recessive hypophosphatemic rickets family carried a mutation affec
31 editary disorders of FGF23 excess that cause hypophosphatemic rickets, has also driven major paradigm
32                                     X-linked hypophosphatemic rickets (HYP) is a dominant disorder ch
33         HHRH is distinct from other forms of hypophosphatemic rickets in that affected individuals pr
34  factor in the pathogenesis of rare forms of hypophosphatemic rickets is rapidly reshaping our unders
35                             In patients with hypophosphatemic rickets, it seems that the dose of phos
36 wly identified disorder, autosomal recessive hypophosphatemic rickets, manifest rickets and osteomala
37 tivity in the pathogenesis of FGF23-mediated hypophosphatemic rickets, more work will need to be done
38 n supplementation can prevent FGF23-mediated hypophosphatemic rickets or osteomalacia.
39  mouse homolog of the human disease X-linked hypophosphatemic rickets/osteomalacia.
40  Additionally, Xpr1-deficient mice developed hypophosphatemic rickets secondary to renal dysfunction.
41 ast growth factor (FGF) 23 causes hereditary hypophosphatemic rickets, such as X-linked hypophosphate
42            A total of 10 adult patients with hypophosphatemic rickets (two males and eight females) w
43 20C conditional knock-out (KO) mice manifest hypophosphatemic rickets, which highlights the crucial r
44           Overexpression of FGF23 results in hypophosphatemic rickets, which is characterized by rena
45                                   Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a
46 e cotransporter 2c (NPT2c), cause hereditary hypophosphatemic rickets with hypercalciuria (HHRH), a d
47 e cotransporter 2c (NPT2c), cause hereditary hypophosphatemic rickets with hypercalciuria (HHRH).
48 n infancy and the treatment of patients with hypophosphatemic rickets with phosphate and vitamin D pr