ライフサイエンスコーパス: bone growth

1 vating mutations in the FGF receptor inhibit bone growth.

2 mesenchyme cells can contribute to calvarial bone growth.

3 th, suggesting that NF-kappaB is involved in bone growth.

4 leading to chondrodysplasia and reduced long bone growth.

5 population determines the rate of calvarial bone growth.

6 promoting as well as inhibiting endochondral bone growth.

7 ammation appears to be necessary for in vivo bone growth.

8 , it is a negative regulator of endochondral bone growth.

9 astatin dose failed to stimulate significant bone growth.

10 98 and indomethacin reduced inflammation and bone growth.

11 are a large family of proteins that promote bone growth.

12 h is the primary determinant of longitudinal bone growth.

13 nvolvement in the regulation of longitudinal bone growth.

14 provide insights regarding the regulation of bone growth.

15 oth embryonic bone development and postnatal bone growth.

16 ates vasorelaxation, cell proliferation, and bone growth.

17 one mineral content, and other parameters of bone growth.

18 his receptor as a negative regulator of long-bone growth.

19 ominant mutation causing a general defect in bone growth.

20 in the growth plate, regulates longitudinal bone growth.

21 lly immature knee and likely reflects normal bone growth.

22 ification in a manner similar to normal long-bone growth.

23 pment, and investigating the biology of long-bone growth.

24 (0.05 mg/kg per day) on muscle accretion and bone growth.

25 eptor genes, both of which are important for bone growth.

26 normal skeletal development and endochondral bone growth.

27 om chondrocytes into bone cells in postnatal bone growth.

28 despite a 35% reduction in the rate of long bone growth.

29 one may play an essential role in regulating bone growth.

30 lamina dura, and radiographical evidence of bone growth.

31 of FGF signaling as a negative regulator of bone growth.

32 e growth plate, ultimately inhibiting linear bone growth.

33 role for FGFRs in the negative regulation of bone growth.

34 ation of the rate and extent of endochondral bone growth.

35 sia with enhanced and prolonged endochondral bone growth.

36 e mass and increased longitudinal and radial bone growth.

37 n the growth plate and improved endochondral bone growth.

38 iferation and the regulation of longitudinal bone growth.

39 ght and bone mass, and impaired longitudinal bone growth.

40 ed in columns along the longitudinal axis of bone growth.

41 vity, resulting in attenuation of periosteal bone growth.

42 y regulates growth plate activity and linear bone growth.

43 tal disorders that feature poor endochondral bone growth.

44 demonstrate a similar defect in endochondral bone growth.

45 e height, resulting in enhanced longitudinal bone growth.

46 development and function, wound healing, and bone growth.

47 e to dietary sodium and calcium during rapid bone growth.

48 osaurid caudal centrum, surrounded by healed bone growth.

49 process of differentiation, regulating long bone growth.

50 n D status are both needed to maximize fetal bone growth.

51 CNP analog led to a significant recovery of bone growth.

52 genitor stem cells capable of supporting new bone growth.

53 tion and differentiation during longitudinal bone growth.

54 tion reverberate on, and delay, overall long bone growth.

55 st in its potential clinical application for bone growth.

56 of chondrocyte hypertrophy and endochondral bone growth.

57 side of the growth plate during endochondral bone growth.

58 epleting chondrocytes needed for normal long bone growth.

59 stimulating the Wnt pathway for therapeutic bone growth.

60 including inflammation, hemorrhage, and new bone growth.

61 ification centers and limit the endochondral bone growth.

62 cell proliferation and ultimately regulates bone growth.

63 ryos, defective mineralization and decreased bone growth accompanied deficient Mmp-13 and Col10a1 gen

64 hydroxyvitamin D [25(OH)D] status, and fetal bone growth across pregnancy.

65 ow that CMP-based probes can detect abnormal bone growth activity in a mouse model of Marfan syndrome

66 has been shown to stimulate murine calvarial bone growth after multiple injections.

67 during late puberty to young adulthood, when bone growth and accrual decelerate.

68 ism to regulate the enzyme's activity during bone growth and aging, two processes known for significa

69 role of BMP receptor signaling in postnatal bone growth and bone formation in vivo.

70 ed signals from the knee joint that modulate bone growth and could underlie establishment of body pro

71 growth factors (FGF) play a critical role in bone growth and development affecting both chondrogenesi

72 viduals with autosomal dominant disorders of bone growth and development provide a unique opportunity

73 ed further analysis of its role in postnatal bone growth and development.

74 potentially mediated through alterations in bone growth and development.

75 -2), an important modulator of cartilage and bone growth and differentiation, is expressed and regula

76 , TGF-beta 1, and bFGF) on the regulation of bone growth and differentiation.

77 sease characterized by delayed and irregular bone growth and early-onset osteoarthritis.

78 food restriction is associated with reduced bone growth and growth hormone (GH) insensitivity.

79 y of Ihh, results in suppressed longitudinal bone growth and growth plate chondrogenesis.

80 ssential multifunctional player in postnatal bone growth and homeostasis.

81 about the mechanism by which FGFR3 inhibits bone growth and how FGFR3 signaling interacts with other

82 process requiring specific cues for optimal bone growth and implant fixation.

83 r Osx has an essential function in postnatal bone growth and in bone homeostasis.

84 ine family, has been implicated in excessive bone growth and in the process of fibrosis.

85 ondral ossification, leading to stunted long bone growth and increased pathologic neovascularization

86 n methylcellulose gel was shown to stimulate bone growth and inflammation over mouse calvaria and in

87 en demonstrated that Sr(2+) ions can promote bone growth and inhibit bone resorption.

88 Boron may be beneficial for bone growth and maintenance, central nervous system func

89 x5 exerts in part its key regulatory role in bone growth and maturation by controlling via Cx40 the e

90 et-derived growth factor gene, which affects bone growth and may influence differences in body size b

91 porary exposure to adiponectin deficiency on bone growth and metabolism.

92 in children and adolescents, optimization of bone growth and mineral accrual for life, pediatric bone

93 ife may be a sensitive period in relation to bone growth and mineralization during childhood.We exami

94 he control of endochondral ossification, and bone growth and mutations that cause hyperactivation of

95 ng in bone are necessary to establish radial bone growth and optimize mineral acquisition during grow

96 ly selected young children, while preserving bone growth and organ function.

97 sagittal synostosis) demonstrated continuous bone growth and overlapping sagittal sutures.

98 shortened limbs due to retarded endochondral bone growth and premature closure of cranial base syncho

99 Bone growth and remodeling depend upon the opposing rate

100 r of osteoclast maturation, yet its roles in bone growth and remodeling have not been assessed, as ma

101 Bone growth and remodeling is inhibited by denervation i

102 ranscription factors with important roles in bone growth and repair.

103 , yet it does not appear to be essential for bone growth and skeletal development.

104 maintenance of skeletal integrity, impaired bone growth and strength, particularly in limb bones, re

105 of circulating IGF-1 is necessary for normal bone growth and suggests that IGF-1, IGFBP-3, and ALS pl

106 s likely to be the cause of disrupted linear bone growth and the resulting short-limbed dwarfism in t

107 Early-life PAT accelerates total mass and bone growth, and causes progressive changes in gut micro

108 Longitudinal bone growth, and hence stature, are functions of growth

109 peptide receptor B or NPR2, stimulates long bone growth, and missense mutations in GC-B cause dwarfi

110 ress markers such as Bip and Atf4, increased bone growth, and reduced skeletal dysplasia.

111 ndochondral, periosteal, and intramembranous bone growth are not known.

112 edundancy and feedback mechanisms regulating bone growth are poorly understood.

113 mutations of FGFR3, a negative regulator of bone growth, are well known to cause a variety of short-

114 skeletal ciliopathies suffer from premature bone growth arrest, mirroring skeletal features associat

115 gene develop unusual lesions of heterotopic bone growth associated with mixed tumor formation arisin

116 Unwanted bone growth beyond the defect margin anteriorly was sign

117 strate that rhBMP-2 can be used to stimulate bone growth both around and onto the surface of endosseo

118 nd articular chondrocytes, not only for long bone growth, but also for bone remodeling.

119 nd via locally generated IGF-I, can regulate bone growth, but at the expense of diabetogenic, lipolyt

120 c fronts is the main mechanism for calvarial bone growth, but importantly, we show that suture mesenc

121 ndrogenesis during development and postnatal bone growth, but the control mechanisms of BMP-2 express

122 te chondrocytes is required for endochondral bone growth, but the mechanisms and pathways that contro

123 data suggest that Igf1 promotes longitudinal bone growth by 'insulin-like' anabolic actions which aug

124 Ihh in chondrocytes that paces longitudinal bone growth by controlling growth plate chondrocyte prol

125 is a modulator of the negative regulation of bone growth by FGF in vivo.

126 owth, strongly suggesting that regulation of bone growth by FGFR3 is mediated at least in part by the

127 growth plate chondrogenesis and longitudinal bone growth by inducing BMP-2 expression and activity.

128 st a model in which Fgfr3 signaling inhibits bone growth by inhibiting chondrocyte differentiation th

129 We found that FGFR3 inhibited endochondral bone growth by markedly inhibiting chondrocyte prolifera

130 ation, thereby indicating that IGF2 controls bone growth by regulating glucose metabolism in chondroc

131 1 (Igf1) is reputed to augment longitudinal bone growth by stimulating growth plate chondrocyte prol

132 in the growth plate accelerates longitudinal bone growth by stimulating growth plate chondrogenesis.

133 rP partially reversed the inhibition of long bone growth caused by activation of FGFR3; however, it i

134 g affects endochondral ossification and long bone growth, causing several genetic forms of human dwar

135 At 35 days, BMP35f developed greater bone growth compared with all other groups including BMP

136 Results: At 10 days, CONe developed greater bone growth compared with CONf (P<0.05), while both BMP

137 that proteins called c-type lectins promote bone growth could lead to new treatments for age-related

138 r 2 (FGF2) signaling plays a pivotal role in bone growth/differentiation through the activation of os

139 rmine whether cholesterol deficiency affects bone growth directly at the growth plate, we then cultur

140 ngs indicate that STC1 inhibits longitudinal bone growth directly at the growth plate.

141 te maturation, leading to the nanomelic long bone growth disorder.

142 odule is not limited to this second phase of bone growth: during later larval development, the Op is

143 rd of the animals formed one or more ectopic bone growths (exostoses).

144 cytes, which form the scaffold on which long bone growth extends, are reduced in linear dimension by

145 nic bovine bone and that this combination of bone growth factor and mineral matrix has the potential

146 collagen matrix and that this combination of bone growth factor and mineral-collagen matrix has the p

147 For example, the bone growth factor BMP2 was locally attached to the coat

148 ic proteins (BMPs) are an important class of bone growth factors and will be the focus of this articl

149 The advent of bone growth factors has been widely anticipated since th

150 ed OPG in osteoclast formation and postnatal bone growth has not been directly investigated.

151 decade, no effective therapies to stimulate bone growth have emerged.

152 c peptide receptor B (NPR-B) stimulates long bone growth in a C-type natriuretic peptide-dependent ma

153 mechanism responsible for poor endochondral bone growth in achondroplasia disorders caused by mutati

154 n physically as a nidus for appositional new bone growth in alveolar sockets following tooth extracti

155 ffect of HIV infection on calcium status and bone growth in children.

156 ested to act as a negative regulator of long-bone growth in chrondrocytes, it produces differentiativ

157 ith the in vivo observations, FGF2 inhibited bone growth in culture and induced downregulation of IHH

158 ew studies have addressed calcium status and bone growth in HIV-infected children.

159 We evaluated fetal long bone growth in human immunodeficiency virus (HIV)-infect

160 importance of maternal zinc status for fetal bone growth in humans and illustrate the value of ultras

161 show that enhanced mTORC1 signaling arrests bone growth in lysosomal storage disorders (LSDs).

162 angiogenesis, ossification, and longitudinal bone growth in mice.

163 ed rat uterus but did not affect TAM-induced bone growth in ovariectomized rats.

164 d simvastatin (SIM) has been shown to induce bone growth in rat models.

165 nthase inhibitors on tissue inflammation and bone growth in rats and gene expression in mice.

166 s the primary cause of retarded longitudinal bone growth in TDII.

167 ceed and significantly improved endochondral bone growth in TDII.

168 caused reduced trabecular and cortical long bone growth in vivo.

169 ion temperature influences motility and limb bone growth in West African Dwarf crocodiles, producing

170 ntable skeletal syndrome that reduced radial bone growth, increased numbers of bone-resorbing periost

171 ments the early effects of BMP-2-induced new bone growth indicating remodeling to physiological level

172 s promoter is sufficient to enhance parietal bone growth into the sagittal suture by P6.

173 Postnatal bone growth involves a dramatic increase in length and g

174 Bone growth is driven by cell proliferation and the subs

175 Bone growth is influenced by dietary intake, particularl

176 e two signaling systems interact to regulate bone growth is poorly understood.

177 echanism by which FGFs regulate endochondral bone growth is through their inhibitory effect on chondr

178 analysed the delta(15) N values from annual bone growth layer rings from dead-stranded animals, and

179 attachment level (CAL) >/=2.7 mm and linear bone growth (LBG) >/=1.1 mm.

180 ecession (GR) measured clinically and linear bone growth (LBG) and percent bone fill (% BF) as assess

181 Therefore, its regulatory effects on bone growth likely result from cellular contexts and not

182 s in the Wnt pathway have been implicated in bone growth, mediation of fibroblast activity, and have

183 D3) plays a major role in the stimulation of bone growth, mineralization, and intestinal calcium and

184 genetic mouse model to study extrinsic long bone growth modulation, in which injury is specifically

185 Bone growth needs in 1-4-y-old children following Americ

186 g/d, which is the amount that meets expected bone growth needs in children of this age.

187 scaffold upon which subsequent longitudinal bone growth occurs.

188 attachment of 1.5 mm was used with a linear bone growth of 2.5 mm, a dose response pattern detected

189 use of rhPDGF-BB led to an increased rate of bone growth of approximately 2 mm compared to the osseoc

190 Yet, it is not clear whether the reduced bone growth of these mice depends on the lack of NF-kapp

191 Simvastatin has been shown to stimulate new bone growth on rat mandibles, but much of the bone is lo

192 ment in CAL and either improvement in linear bone growth or percent bone fill.

193 Sclerosteosis, another disorder of excessive bone growth, our study suggests that the SOST-LRP5 antag

194 th inhibition by acting directly at the long bones' growth plate.

195 nically acceptable level without sacrificing bone-growth potential, but COX-associated inflammation a

196 llowed by capillary invasion, restoration of bone growth, resorption of the hypertrophic cartilage an

197 Activating mutations severely limit bone growth, resulting in dwarfism, while inactivating m

198 n have exhibited only minimal or none of the bone growth retardation expected with EBRT.

199 e (HA), and a focal point substituted with a bone growth stimulating peptide (BMP2), has been compreh

200 of 0.001 which is of particular interest for bone growth stimulation is achievable by this assembly.

201 r 3 (FGFR3) is a major negative regulator of bone growth that inhibits the proliferation and differen

202 ive zone and by acceleration of longitudinal bone growth, that attenuated as the animals grew older.

203 signaling in diverse processes ranging from bone growth to stem cell activity.

204 ypertrophic differentiation and the improved bone growth was associated with increased chondrocyte pr

205 Bone growth was associated with the induction of osteocl

206 surrounding postnatal GPs were killed, left bone growth was nevertheless reduced.

207 homozygous skeletons was sparse, but overall bone growth was unaffected.

208 odulin-1, a known regulator of cartilage and bone growth, was expressed at high levels specifically i

209 growth plate chondrogenesis and longitudinal bone growth, we chose an organ culture model.

210 Significant differences in radial bone growth were present between the groups.

211 attenuation of longitudinal vertebra or limb-bone growth were seen in null animals.

212 Simvastatin has been shown to increase bone growth when applied topically to murine bone; howev

213 growth plate chondrogenesis and longitudinal bone growth with its stimulatory effects primarily media

214 ion of chondrocytes and negatively regulates bone growth without inhibiting chondrocyte proliferation