ライフサイエンスコーパス: bone mineralization

1 or-alpha heterodimer (VDRRXRalpha) regulates bone mineralization.

2 ed arterial calcification but did not affect bone mineralization.

3 valve calcification analogous to physiologic bone mineralization.

4 aired osteoblast differentiation and reduced bone mineralization.

5 lance in early life may influence subsequent bone mineralization.

6 ole for of pth4-expressing neurons in larval bone mineralization.

7 ctor-23) regulates phosphate homeostasis and bone mineralization.

8 h neurofibromin as an essential regulator of bone mineralization.

9 essential for osteoblast differentiation and bone mineralization.

10 ng that PTHrP could contribute to the excess bone mineralization.

11 ith hypovitaminosis D presented with delayed bone mineralization.

12 with elevated bone resorption and decreased bone mineralization.

13 assessed for alkaline phosphatase (ALP) and bone mineralization.

14 se may reflect small body size or suboptimal bone mineralization.

15 and collagen I, the structural template for bone mineralization.

16 expressed in osteoblasts and contributes to bone mineralization.

17 luate the possible role of this mechanism in bone mineralization.

18 oesophageal reflux, bacterial infection, and bone mineralization.

19 ies provide an insight into the mechanism of bone mineralization.

20 between cortical porosity and the degree of bone mineralization.

21 pression, leading to pathological changes in bone mineralization.

22 tamin K can result in abnormal cartilage and bone mineralization.

23 minosis D) causes osteomalacia and poor long bone mineralization.

24 sts, and its disruption results in defective bone mineralization.

25 l role for hydroxylated collagen proteins in bone mineralization.

26 rge, through expected term, further improved bone mineralization.

27 ereas its expression in osteoblasts prevents bone mineralization.

28 PP(i) concentrations required for controlled bone mineralization.

29 n D deficiency are associated with decreased bone mineralization.

30 isphosphonate etidronate that inhibit normal bone mineralization.

31 re potent and do not have adverse effects on bone mineralization.

32 ed susceptibility to infection and decreased bone mineralization.

33 Here, we show the respective correction of bone mineralization abnormalities in knockout mice null

34 onal extracutaneous features such as loss of bone mineralization and abnormal teeth, as well as a res

35 r breast-milk calcium concentration, and the bone mineralization and blood pressure of her infant, bu

36 ed the number of rib fractures, and improved bone mineralization and bone cortical thickness.

37 e mass, microarchitecture, and the degree of bone mineralization and elastic modulus within the trabe

38 dings demonstrate the importance of NCX1 for bone mineralization and explain why deletion of an ion c

39 and DMP1 control a common pathway regulating bone mineralization and FGF23 production, the latter inv

40 Vitamin D regulates bone mineralization and is associated with pleiotropic e

41 s facilitates the role of the endothelium in bone mineralization and morphogenesis.

42 There was no decrease in bone mineralization and no increase in proliferation of

43 s of the human disease, including diminished bone mineralization and propensity to fracture.

44 genes is necessary and sufficient to induce bone mineralization and provides evidence that pathologi

45 release abnormal humoral factors that affect bone mineralization and proximal tubule phosphate transp

46 of skeletal features and an indicator of the bone mineralization and remodeling processes.

47 The process of bone mineralization and resorption is complex and is aff

48 Because of the resulting increase in bone mineralization and sclerosis, the osteoblastic proc

49 Such bone remodeling caused disturbed bone mineralization and severe bone loss, as reported in

50 -beta 2 overexpression resulted in defective bone mineralization and severe hypoplasia of the clavicl

51 ,25-dihydroxyvitamin D3, along with abnormal bone mineralization and soft tissue calcifications.

52 The short stature and impaired bone mineralization and strength in mice lacking Nf1 in

53 A pathologic link between abnormal bone mineralization and VC through the serum phosphorus

54 charge shows no advantage over TF in growth, bone mineralization, and body composition.

55 r energy metabolism, nucleic acid synthesis, bone mineralization, and cell signaling.

56 ment characteristics, laboratory measures of bone mineralization, and dietary intake.

57 Linear growth, bone mineralization, and fracture rate were taken as mea

58 rate proteins involved in blood coagulation, bone mineralization, and signal transduction and inverte

59 t, derangements in and treatment of abnormal bone mineralization, and transitional care issues; the l

60 concentrations in preterm infant formula on bone mineralization are lacking, recommendations for the

61 Chondrocyte maturation and bone mineralization are severely compromised in Mia3-nul

62 tide hormone, phosphatonin, which suppresses bone mineralization as well as renal phosphate reabsorpt

63 trations during late pregnancy and offspring bone mineralization assessed at birth with the use of du

64 Bone mineralization at hospital discharge and expected t

65 he data show that sclerostin not only alters bone mineralization, but also influences mineral metabol

66 SSRIs (except citalopram) inhibited ALP and bone mineralization by OB but only at 30 mumol/L.

67 clear how a lack of Ano6 leads to a delay in bone mineralization by osteoblasts.

68 ulator of calcium/phosphorous metabolism and bone mineralization-can exert effects on cells of the im

69 growth factor (IGF)-1 in growth control and bone mineralization, circulating IGF-1 levels in the ser

70 Inhibitors of bone mineralization completely prevented ectopic cardiac

71 R signaling and greatly reduced capacity for bone mineralization, contributing to profound skeletal d

72 protein DMP1 result in equivalent intrinsic bone mineralization defects and increased Fgf23 expressi

73 n addition, Mepe-deficient Hyp mice retained bone mineralization defects in vivo, characterized by de

74 Despite alveolar bone mineralization defects, periodontal attachment and

75 dicate that in normal individuals, decreased bone mineralization does not appear to affect final grow

76 t preterm infants undergo catch-up growth in bone mineralization during infancy.

77 ly increases calcium absorption and enhances bone mineralization during pubertal growth.

78 in JRA appear to exert a negative effect on bone mineralization even in prepubertal children, which

79 e been used effectively for the detection of bone mineralization, growth, and morphological changes.

80 ue mineralization while correcting decreased bone mineralization in generalized arterial calcificatio

81 ata suggest an association between decreased bone mineralization in JRA and low bone formation that i

82 cellular stress and indeed 4PBA ameliorated bone mineralization in larvae and skeletal deformities i

83 Because melatonin has been shown to affect bone mineralization in other animals, we examined whethe

84 ngs were tolerated through expected term, on bone mineralization in preterm infants.

85 other organs to adjust phosphate balance and bone mineralization in response to changing physiologica

86 d phosphorus are accreted to enable enhanced bone mineralization in the absence of sclerostin, we mea

87 Bone mineralization is an essential step during the embr

88 Cementum and bone mineralization is regulated by factors including en

89 established well before the rapid growth and bone mineralization observed in adolescence.

90 Expression of bone mineralization regulating genes Mmp13, Ocn, Osx and

91 transplantation, and hepatitis C can affect bone mineralization, remodeling, or bone mass.

92 ist; however, patients at risk for decreased bone mineralization should be screened and treated to pr

93 (-/-) mice featured disturbances in alveolar bone mineralization, shown by accumulation of unminerali

94 me that is induced upon injury and regulates bone mineralization, significantly attenuated cardiac ca

95 y suffer additional morbidity from decreased bone mineralization, such as skeletal fracture.

96 y demonstrate a regulatory role for CD40L in bone mineralization that is absent in patients with X-li

97 s critical to understanding the mechanism of bone mineralization, there have been as yet no studies o

98 Vitamin D is also known to be important in bone mineralization; thus, 1,25-vitamin D may be one fac

99 or-alpha heterodimer (VDRRXRalpha) regulates bone mineralization via transcriptional control of osteo

100 ney axis and new systems biology that govern bone mineralization, vitamin D metabolism, parathyroid g

101 Bone mineralization was delayed in 48% of the patients,

102 enes expressed in osteocytes associated with bone mineralization was significantly higher at the late

103 mouse with a perinatal phenotype of delayed bone mineralization which was resolved by 1 month.

104 and VI osteogenesis imperfecta via defective bone mineralization, while defects in cartilage-associat

105 ular phosphate concentration is required for bone mineralization, while lowering this concentration p