ライフサイエンスコーパス: bone growth

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

2 st in its potential clinical application for bone growth.

3 of chondrocyte hypertrophy and endochondral bone growth.

4 side of the growth plate during endochondral bone growth.

5 epleting chondrocytes needed for normal long bone growth.

6 stimulating the Wnt pathway for therapeutic bone growth.

7 including inflammation, hemorrhage, and new bone growth.

8 ification centers and limit the endochondral bone growth.

9 cell proliferation and ultimately regulates bone growth.

10 mesenchyme cells can contribute to calvarial bone growth.

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

12 leading to chondrodysplasia and reduced long bone growth.

13 population determines the rate of calvarial bone growth.

14 promoting as well as inhibiting endochondral bone growth.

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

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

17 astatin dose failed to stimulate significant bone growth.

18 98 and indomethacin reduced inflammation and bone growth.

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

20 h is the primary determinant of longitudinal bone growth.

21 nvolvement in the regulation of longitudinal bone growth.

22 provide insights regarding the regulation of bone growth.

23 oth embryonic bone development and postnatal bone growth.

24 ates vasorelaxation, cell proliferation, and bone growth.

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

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

27 for resorbing cartilage to lead directional bone growth.

28 ominant mutation causing a general defect in bone growth.

29 in the growth plate, regulates longitudinal bone growth.

30 lly immature knee and likely reflects normal bone growth.

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

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

33 (0.05 mg/kg per day) on muscle accretion and bone growth.

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

35 normal skeletal development and endochondral bone growth.

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

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

38 vating mutations in the FGF receptor inhibit bone growth.

39 lamina dura, and radiographical evidence of bone growth.

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

41 e growth plate, ultimately inhibiting linear bone growth.

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

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

44 sia with enhanced and prolonged endochondral bone growth.

45 endothelium lacking the capacity to promote bone growth.

46 ate neighboring skull bones and are sites of bone growth.

47 ered cartilage cytoarchitecture and impaired bone growth.

48 plate maintenance and prolonged longitudinal bone growth.

49 -1) axis, which is critical for longitudinal bone growth.

50 aling interacts in regulating the periosteal bone growth.

51 rtilage-to-bone transition, and longitudinal bone growth.

52 icular hypertrophy, fat metabolism, and long bone growth.

53 morphogenesis throughout pre- and postnatal bone growth.

54 bone formation while diminishing periosteal bone growth.

55 cture recovered, including partial rescue of bone growth.

56 genes known to be important in longitudinal bone growth.

57 e coronal suture and contribute to calvarial bone growth.

58 nergize to cause reduced and dysmorphic limb bone growth.

59 ex and also as the site for endochondral jaw bone growth.

60 om chondrocytes into bone cells in postnatal bone growth.

61 e mass and increased longitudinal and radial bone growth.

62 n the growth plate and improved endochondral bone growth.

63 iferation and the regulation of longitudinal bone growth.

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

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

66 vity, resulting in attenuation of periosteal bone growth.

67 y regulates growth plate activity and linear bone growth.

68 tal disorders that feature poor endochondral bone growth.

69 demonstrate a similar defect in endochondral bone growth.

70 e height, resulting in enhanced longitudinal bone growth.

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

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

73 osaurid caudal centrum, surrounded by healed bone growth.

74 process of differentiation, regulating long bone growth.

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

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

77 genitor stem cells capable of supporting new bone growth.

78 tion and differentiation during longitudinal bone growth.

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

80 Longitudinal bone growth, achieved through endochondral ossification,

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

82 ansforms type H vessels into type L to limit bone growth activity and enhance bone mineralization.

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

84 e (TIMP) gene family is essential for normal bone growth after birth.

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

86 d treatment with GCs is well known to impair bone growth, an effect linked to increased apoptosis and

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

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

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

90 didate genes believed to affect longitudinal bone growth and bone mass.

91 lume, abnormal swim movement, and defects in bone growth and composition.

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

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

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

95 s of the major pathway genes associated with bone growth and development, particularly craniofacial (

96 potentially mediated through alterations in bone growth and development.

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

98 rrow adiposity may have a negative effect on bone growth and development.

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

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

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

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

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

104 with functions in the human body related to bone growth and homeostasis.

105 ssential multifunctional player in postnatal bone growth and homeostasis.

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

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

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

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

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

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

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

113 is a key systemic regulator of longitudinal bone growth and is widely used in pediatric endocrinolog

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

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

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

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

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

119 As a result, YNVs promote longitudinal bone growth and mineral density of the tibia in the OVX-

120 Ibsp in mice (Ibsp(-/-)) results in impaired bone growth and mineralization and defective osteoclasto

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

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

123 These proteins included mediators of bone growth and neurodevelopment.

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

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

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

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

128 entral ERalpha-signaling limits longitudinal bone growth and radial bone expansion specifically in fe

129 Bone growth and remodeling depend upon the opposing rate

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

131 Bone growth and remodeling is inhibited by denervation i

132 y osteochondral SSC (ocSSC) facilitates long bone growth and repair, while a second type, a perivascu

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

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

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

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

137 ation of these cells determines longitudinal bone growth and the matrix deposited provides a scaffold

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

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

140 e healing, medications used postoperatively, bone growth, and density changes as quantified on a cone

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

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

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

144 , including the rate of frontal and parietal bone growth, and the boundary between sutural and osteog

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

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

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

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

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

150 ancer-secreted factors may promote perturbed bone growth before metastasis, which could affect initia

151 Unwanted bone growth beyond the defect margin anteriorly was sign

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 1 (Igf1) is reputed to augment longitudinal bone growth by stimulating growth plate chondrocyte prol

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

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

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

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

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

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

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

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

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

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

177 clear benefits to select patients with rare bone growth disorders, acute promyelocytic leukemia, and

178 educed body size, and defective endochondral bone growth due to impaired BMP-mediated chondrogenesis

179 try of T. tumanovae resulted from restricted bone growth due to tail club strikes.

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

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

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

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

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

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

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

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

188 coloration; enamel hypoplasia; inhibition of bone growth following use in late pregnancy, infancy, or

189 ogenicity, high production cost, and ectopic bone growth from these therapies remain.

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

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

192 H vessel identity and thus limit adolescent bone growth have remained ill defined.

193 Interestingly, GC-induced bone growth impairment and chondrocyte apoptosis was pre

194 new possible strategy to prevent GC-induced bone growth impairment by cotreating with HN.

195 ulator of Hh signaling preventing GC-induced bone growth impairment without interfering with desired

196 ignaling and prevents glucocorticoid-induced bone growth impairment.

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

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

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

200 Longitudinal bone growth in children is sustained by growth plates, n

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

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

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

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

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

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

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

208 n of neuronal ERalpha had no major effect on bone growth in males.

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

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

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

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

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

214 ceed and significantly improved endochondral bone growth in TDII.

215 expression of Wnt7b fully rescues periosteal bone growth in the Bmpr1a-deficient mice.

216 sulted in significant increases in postnatal bone growth in the first 6 months of life for both male

217 nt in vitro; however, statins did not impair bone growth in vivo due to insufficient penetration into

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

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

220 d to treat MB, cause irreversible defects in bone growth in young children.

221 transcription factors of known importance to bone growth, including SOX6, SOX9 and RUNX2.

222 reatment with 8n or 13a also enhanced linear bone growth, increased mineralization of bone, and narro

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

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

225 ither increase or decrease expression of the bone growth inhibitor gene Stanniocalcin2a in developing

226 Histology confirmed bone growth inside the porous 3D scaffolds with or witho

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

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

229 Bone growth is driven by cell proliferation and the subs

230 Bone growth is influenced by dietary intake, particularl

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

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

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

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

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

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

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

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

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

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

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

242 scaffold upon which subsequent longitudinal bone growth occurs.

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

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

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

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

247 ined the effects of peripartum SSRIs on long bone growth or mass.

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

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

250 emilunar heart valves, but they did not have bone growth plate defects.

251 nto four anatomical compartments, epiphyseal bone, growth plate, primary spongiosa, and secondary spo

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

253 hondrocytes, cartilage cells comprising long-bone growth plates.

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

255 Bone growth requires a specialised, highly angiogenic bl

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

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

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

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

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

261 Noninvasive electronic bone growth stimulators (EBGSs) have been in clinical us

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

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

264 ow that selection may favor de-repression of bone growth through inactivating two limb enhancers of a

265 ome and Brachydactyly Type B1, which disrupt bone growth throughout the endochondral skeleton.

266 in addition to their known requirements for bone growth throughout the skeleton.

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

268 eately enhanced by continuous stimulation of bone growth using systemic administration of fracture-ta

269 results in temporal and long-term changes in bone growth via regulation of bone formation.

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

271 Bone growth was associated with the induction of osteocl

272 ; however, in the majority of cases, the new bone growth was at a distance from the implant surface w

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

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

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

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

277 has been linked to osteoporosis and impaired bone growth, we hypothesized that the ability of teleost

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

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

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

281 bited a significant increase in appositional bone growth, which increased the height and width of the

282 osteogenic activity is controlled to promote bone growth while preventing aberrant bone fusions durin

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

284 They also had retinal dysplasia and abnormal bone growth, with a narrowed thorax and short ribs, shor

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