ライフサイエンスコーパス: hypophosphatemic rickets

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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

13 X-linked hypophosphatemic rickets, a dominantly inherited disease

14 Autosomal dominant hypophosphatemic rickets (ADHR) is an inherited disorder

15 Autosomal dominant hypophosphatemic rickets (ADHR) is unique among the diso

16 The metabolic disorder autosomal dominant hypophosphatemic rickets (ADHR) was previously mapped to

17 In the Hyp-mouse homologue of X-linked hypophosphatemic rickets, administration of 1,25(OH)(2)D

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

24 cise mechanisms of how excess FGF23 leads to hypophosphatemic rickets are not clear.

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

27 An adolescent with hypophosphatemic rickets developed cardiac calcification

28 nal analyses showed that autosomal recessive hypophosphatemic rickets family carried a mutation affec

29 X-linked hypophosphatemic rickets (HYP) is a dominant disorder ch

30 HHRH is distinct from other forms of hypophosphatemic rickets in that affected individuals pr

31 factor in the pathogenesis of rare forms of hypophosphatemic rickets is rapidly reshaping our unders

32 In patients with hypophosphatemic rickets, it seems that the dose of phos

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

35 mouse homolog of the human disease X-linked hypophosphatemic rickets/osteomalacia.

36 Additionally, Xpr1-deficient mice developed hypophosphatemic rickets secondary to renal dysfunction.

37 A total of 10 adult patients with hypophosphatemic rickets (two males and eight females) w

38 20C conditional knock-out (KO) mice manifest hypophosphatemic rickets, which highlights the crucial r

39 Overexpression of FGF23 results in hypophosphatemic rickets, which is characterized by rena

40 Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is a

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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