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1 ine-1-phosphate acts in paracrine to promote bone mineralization.
2 PP(i) concentrations required for controlled bone mineralization.
3 n D deficiency are associated with decreased bone mineralization.
4 isphosphonate etidronate that inhibit normal bone mineralization.
5 re potent and do not have adverse effects on bone mineralization.
6 ed susceptibility to infection and decreased bone mineralization.
7 valve calcification analogous to physiologic bone mineralization.
8 , including those relating to gut health and bone mineralization.
9 se and causally associated with disorders of bone mineralization.
10 or-alpha heterodimer (VDRRXRalpha) regulates bone mineralization.
11 chemical analysis were used to assess TP and bone mineralization.
12  1, previously identified as a key factor in bone mineralization.
13 ated the number of SPCs, bone formation, and bone mineralization.
14  L to limit bone growth activity and enhance bone mineralization.
15 ry shows increased osteoblasts but decreased bone mineralization.
16 ole for of pth4-expressing neurons in larval bone mineralization.
17 rioration in histomorphometric parameters of bone mineralization.
18  N230, N271, N303, N430) that is crucial for bone mineralization.
19 iomechanical properties and increased callus bone mineralization.
20 wave of calcium uptake necessary to initiate bone mineralization.
21 viously undescribed requirement for Sox10 in bone mineralization.
22 minosis D) causes osteomalacia and poor long bone mineralization.
23 ed arterial calcification but did not affect bone mineralization.
24 aired osteoblast differentiation and reduced bone mineralization.
25 lance in early life may influence subsequent bone mineralization.
26 ctor-23) regulates phosphate homeostasis and bone mineralization.
27 h neurofibromin as an essential regulator of bone mineralization.
28 essential for osteoblast differentiation and bone mineralization.
29 ng that PTHrP could contribute to the excess bone mineralization.
30 ith hypovitaminosis D presented with delayed bone mineralization.
31  with elevated bone resorption and decreased bone mineralization.
32  assessed for alkaline phosphatase (ALP) and bone mineralization.
33 se may reflect small body size or suboptimal bone mineralization.
34 he discovery of polyP as phosphate source in bone mineralization.
35  and collagen I, the structural template for bone mineralization.
36  expressed in osteoblasts and contributes to bone mineralization.
37 luate the possible role of this mechanism in bone mineralization.
38 oesophageal reflux, bacterial infection, and bone mineralization.
39 ies provide an insight into the mechanism of bone mineralization.
40  between cortical porosity and the degree of bone mineralization.
41 pression, leading to pathological changes in bone mineralization.
42 tamin K can result in abnormal cartilage and bone mineralization.
43  structure and dynamics as well as defective bone mineralization.
44 sts, and its disruption results in defective bone mineralization.
45 l role for hydroxylated collagen proteins in bone mineralization.
46 rge, through expected term, further improved bone mineralization.
47 ereas its expression in osteoblasts prevents bone mineralization.
48   Here, we show the respective correction of bone mineralization abnormalities in knockout mice null
49 ut not use of HP dairy products for improved bone mineralization among healthy, well-nourished childr
50 onal extracutaneous features such as loss of bone mineralization and abnormal teeth, as well as a res
51 r breast-milk calcium concentration, and the bone mineralization and blood pressure of her infant, bu
52 ed the number of rib fractures, and improved bone mineralization and bone cortical thickness.
53 e mass, microarchitecture, and the degree of bone mineralization and elastic modulus within the trabe
54 dings demonstrate the importance of NCX1 for bone mineralization and explain why deletion of an ion c
55 and DMP1 control a common pathway regulating bone mineralization and FGF23 production, the latter inv
56                          Vitamin D regulates bone mineralization and is associated with pleiotropic e
57 nherited disorder characterized by defective bone mineralization and is highly variable in its clinic
58    Vitamin D and dairy protein may stimulate bone mineralization and linear growth in children, but p
59 s facilitates the role of the endothelium in bone mineralization and morphogenesis.
60                     There was no decrease in bone mineralization and no increase in proliferation of
61 se abnormalities were suggestive of impaired bone mineralization and normalized at 6 months with corr
62 s of the human disease, including diminished bone mineralization and propensity to fracture.
63  genes is necessary and sufficient to induce bone mineralization and provides evidence that pathologi
64 release abnormal humoral factors that affect bone mineralization and proximal tubule phosphate transp
65 the PC1-CTT into pkd1-morphant fish restores bone mineralization and reduces the severity of the curl
66 ut (Ibsp(-/-)) mice results in developmental bone mineralization and remodeling defects, with alveola
67 of skeletal features and an indicator of the bone mineralization and remodeling processes.
68 e branchpoint depends on the balance between bone mineralization and resorption activities.
69                               The process of bone mineralization and resorption is complex and is aff
70         Because of the resulting increase in bone mineralization and sclerosis, the osteoblastic proc
71        Such bone remodeling caused disturbed bone mineralization and severe bone loss, as reported in
72 -beta 2 overexpression resulted in defective bone mineralization and severe hypoplasia of the clavicl
73 ,25-dihydroxyvitamin D3, along with abnormal bone mineralization and soft tissue calcifications.
74               The short stature and impaired bone mineralization and strength in mice lacking Nf1 in
75 fined our understanding of skull patterning, bone mineralization and tissue homeostasis.
76           A pathologic link between abnormal bone mineralization and VC through the serum phosphorus
77 nition, endothelial dysfunction, hemostasis, bone mineralization, and body composition.
78 charge shows no advantage over TF in growth, bone mineralization, and body composition.
79 r energy metabolism, nucleic acid synthesis, bone mineralization, and cell signaling.
80 ment characteristics, laboratory measures of bone mineralization, and dietary intake.
81                               Linear growth, bone mineralization, and fracture rate were taken as mea
82 rate proteins involved in blood coagulation, bone mineralization, and signal transduction and inverte
83 t, derangements in and treatment of abnormal bone mineralization, and transitional care issues; the l
84 skeletal development, positive regulation of bone mineralization, and wound healing.
85 y enriched in osteoblast differentiation and bone mineralization annotation categories.
86  concentrations in preterm infant formula on bone mineralization are lacking, recommendations for the
87                   Chondrocyte maturation and bone mineralization are severely compromised in Mia3-nul
88 tide hormone, phosphatonin, which suppresses bone mineralization as well as renal phosphate reabsorpt
89 trations during late pregnancy and offspring bone mineralization assessed at birth with the use of du
90                                              Bone mineralization at hospital discharge and expected t
91 he data show that sclerostin not only alters bone mineralization, but also influences mineral metabol
92  SSRIs (except citalopram) inhibited ALP and bone mineralization by OB but only at 30 mumol/L.
93 clear how a lack of Ano6 leads to a delay in bone mineralization by osteoblasts.
94 ulator of calcium/phosphorous metabolism and bone mineralization-can exert effects on cells of the im
95  growth factor (IGF)-1 in growth control and bone mineralization, circulating IGF-1 levels in the ser
96                                Inhibitors of bone mineralization completely prevented ectopic cardiac
97 R signaling and greatly reduced capacity for bone mineralization, contributing to profound skeletal d
98  protein DMP1 result in equivalent intrinsic bone mineralization defects and increased Fgf23 expressi
99 n addition, Mepe-deficient Hyp mice retained bone mineralization defects in vivo, characterized by de
100                             Despite alveolar bone mineralization defects, periodontal attachment and
101 adiography was used to measure the degree of bone mineralization (DMB), and Fourier transform infrare
102 dicate that in normal individuals, decreased bone mineralization does not appear to affect final grow
103 actions will likely reveal new insights into bone mineralization during development.
104 t preterm infants undergo catch-up growth in bone mineralization during infancy.
105 ly increases calcium absorption and enhances bone mineralization during pubertal growth.
106  in JRA appear to exert a negative effect on bone mineralization even in prepubertal children, which
107 uding nucleotide and phospholipid signaling, bone mineralization, fibrotic diseases, and tumor-associ
108 e been used effectively for the detection of bone mineralization, growth, and morphological changes.
109 vious studies identified a role for MEMO1 in bone mineralization; however, whether MEMO1 functions in
110 ation should be the first step in correcting bone mineralization impairment before specific osteoporo
111 ucture and function to the observed abnormal bone mineralization in AIS, which may shed light on etio
112 ibitor (Ac-YVADCMK [AYC]) treatment restores bone mineralization in diabetic mice.
113 ue mineralization while correcting decreased bone mineralization in generalized arterial calcificatio
114 ata suggest an association between decreased bone mineralization in JRA and low bone formation that i
115  cellular stress and indeed 4PBA ameliorated bone mineralization in larvae and skeletal deformities i
116 on in chondrocytes, and cartilage growth and bone mineralization in medaka fish.
117 hich promotes osteoblast differentiation and bone mineralization in mouse and human cell culture mode
118   Because melatonin has been shown to affect bone mineralization in other animals, we examined whethe
119 ngs were tolerated through expected term, on bone mineralization in preterm infants.
120 other organs to adjust phosphate balance and bone mineralization in response to changing physiologica
121 d phosphorus are accreted to enable enhanced bone mineralization in the absence of sclerostin, we mea
122                                              Bone mineralization is an essential step during the embr
123  details remain unclear, initiation of woven bone mineralization is believed to be mediated by collag
124                                 Cementum and bone mineralization is regulated by factors including en
125 established well before the rapid growth and bone mineralization observed in adolescence.
126 calcin determines its essential functions in bone mineralization or systemic metabolism and serves as
127 ns revealed that osteoclast differentiation, bone mineralization, ossification, and myeloid cell deve
128            These new CAC loci are related to bone mineralization, phosphate catabolism and hormone me
129 sis, which is required to facilitate optimal bone mineralization, preserve serum calcium levels withi
130                                Expression of bone mineralization regulating genes Mmp13, Ocn, Osx and
131  transplantation, and hepatitis C can affect bone mineralization, remodeling, or bone mass.
132 mporal disconnects between the peak of total bone mineralization/resorption, and osteoblast/osteoclas
133 ist; however, patients at risk for decreased bone mineralization should be screened and treated to pr
134 (-/-) mice featured disturbances in alveolar bone mineralization, shown by accumulation of unminerali
135 me that is induced upon injury and regulates bone mineralization, significantly attenuated cardiac ca
136 y suffer additional morbidity from decreased bone mineralization, such as skeletal fracture.
137 y demonstrate a regulatory role for CD40L in bone mineralization that is absent in patients with X-li
138 s critical to understanding the mechanism of bone mineralization, there have been as yet no studies o
139 , results in menopausal symptoms and affects bone mineralization, thus limiting treatment duration or
140   Vitamin D is also known to be important in bone mineralization; thus, 1,25-vitamin D may be one fac
141 or-alpha heterodimer (VDRRXRalpha) regulates bone mineralization via transcriptional control of osteo
142 ney axis and new systems biology that govern bone mineralization, vitamin D metabolism, parathyroid g
143                                              Bone mineralization was delayed in 48% of the patients,
144                                      Whereas bone mineralization was normal in all but one patient pr
145 enes expressed in osteocytes associated with bone mineralization was significantly higher at the late
146  mouse with a perinatal phenotype of delayed bone mineralization which was resolved by 1 month.
147 and VI osteogenesis imperfecta via defective bone mineralization, while defects in cartilage-associat
148 ular phosphate concentration is required for bone mineralization, while lowering this concentration p

 
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