ライフサイエンスコーパス: long bone

1 man osteoclasts, rat calvaria, and rat fetal long bone.

2 ng-lived skeletal cells on the periosteum of long bone.

3 expression in joints versus growing ends of long bones.

4 reduced trabecular thickness and density in long bones.

5 re cartilage defects in the growth plates of long bones.

6 s in the growth plate and retarded growth of long bones.

7 ic pubis and clavicles, osteopenia, and bent long bones.

8 craniofacial bones and widened metaphyses in long bones.

9 t to osteochondroma formation, especially in long bones.

10 se (NOMID) develop tumor-like lesions of the long bones.

11 significantly reduced in femoral and tibial long bones.

12 res often restricted to the epiphyses of the long bones.

13 action is more restricted than in wild-type long bones.

14 been developed to correct deformities of the long bones.

15 in mice with targeted deletion of Klotho in long bones.

16 eloped extremely dense, heavily vascularized long bones.

17 sociated with the trabecular bone surface of long bones.

18 immature chondrocytes in the growth plate of long bones.

19 PTH's effect on mkp1 in mouse calvariae and long bones.

20 elopment of bony outgrowths near the ends of long bones.

21 tween the epiphyses and metaphyses of future long bones.

22 cartilaginous anlage and the ossification of long bones.

23 on as measured by calcein incorporation into long bones.

24 erturbed TGF-beta signaling in the skull and long bones.

25 e poorly localized or are localized to major long bones.

26 bones and abnormally developed metaphyses in long bones.

27 a decrease in cortical bone thickness of the long bones.

28 rtical sclerosis of the diaphyses of all the long bones.

29 ccur from the juxtaepiphyseal regions of the long bones.

30 utgrowths from the juxtaepiphyseal region of long bones.

31 maturation of chondrocytes and shortening of long bones.

32 that develop from the growth centers of the long bones.

33 maturation of the cartilage growth plate of long bones.

34 ssification occurring at the ends of growing long bones.

35 of bony protuberances at the ends of all the long bones.

36 by 50%, despite normal Fgf23 mRNA levels in long bones.

37 esponsible for the formation of the skeleton long bones.

38 ble defects of postnatal ossification in the long bones.

39 ary ossification centers (SOCs) of mammalian long bones.

40 phatemia that did not cause major defects in long bones.

41 rotic defects in the diaphysis of the murine long bones.

42 plate regulate postnatal development of the long bones.

43 stem cell (HSC) niche in the bone marrow of long bones.

44 Other phenotypes include shortened long bones, a markedly enlarged spleen, elevated neutrop

45 In long bones, ABM increased three- and sixfold in CBT and

46 The long bone abnormalities in SADDAN mice are milder than t

47 Long-bone abnormalities were identified as early as embr

48 s, and endosteum within the epiphyses of the long bones adjacent to articular joints.

49 rmed after skeletal scintigraphy shows major-long-bone AHO if treatment response is slow.

50 ge were found in 3 (6%) of 48 cases of major-long-bone AHO.

51 Mysm1-/- mice had a lower bone mass both in long bone and calvaria compared with their control count

52 articular cartilage destruction and abnormal long bone and craniofacial development.

53 ondrocytes into bone cells is common in both long bone and mandibular condyle development and during

54 gressive foreshortening and deformity of the long bones and axial skeleton but apparently normal toot

55 Long bones and calvariae of TG mice showed reduced COL1A

56 al similarities, including shortening of the long bones and constriction of the thoracic cage.

57 all epiphysis, slightly flared metaphysis of long bones and flattened vertebrae, characteristic of sp

58 Dwarfism disproportionately affects long bones and is characterized by a defect in the proli

59 ng limb mesenchyme results in defects in the long bones and joints of mice.

60 in dogs is defined by dysplastic, shortened long bones and premature degeneration and calcification

61 ore, destruction of the articular surface in long bones and premature fusion of growth plates of vari

62 including disorganization of chondrocytes in long bones and premature hypertrophy in costochondral ca

63 led (Fzd) signaling alters the dimensions of long bones and produces cell-autonomous changes in proli

64 sclerosing skeletal dysplasia affecting the long bones and skull.

65 is and chondrocyte hypertrophy in developing long bones and suggests that a novel transcriptional rep

66 for the osteoblast lineage in the developing long bones and that Ihh functions in conjunction with ot

67 Long bones and the cranial base are both formed through

68 that varied from the rare chondromas in the long bones and the ubiquitous osteochondrodysplasia of v

69 ne mass, with increased cortical porosity in long bones and thinner flat bones in the skull.

70 c metaphyses with persistence of club-shaped long bones and unerupted teeth, and the growth plate def

71 2 months, which continued up to 8 months in long bones and vertebrae, but not calvariae.

72 rooked tails and curvature and overgrowth of long bones and vertebrae.

73 n-2 (rhBMP-2) has been introduced for spine, long bone, and craniofacial indications.

74 esorption in the subepiphyseal region of the long bone, and incomplete correction of the hematologic

75 seal plate function, constrain the growth of long bones, and prevent attainment of a high peak bone m

76 ferent manner than the more sparsely jointed long bones, and their identity is regulated by different

77 anking the epiphyseal region of mouse embryo long bone anlagen - a region encompassing the groove of

78 During limb skeletogenesis the cartilaginous long bone anlagen and their growth plates become delimit

79 s observed when HS function was disrupted in long bone anlagen explants by genetic, pharmacological o

80 Limb long bone anlagen were entirely composed of chondrocytes

81 ferior material properties of Pcolce-/- male long bone, apparently compensated for by the adaptive ch

82 eogenesis has been successfully employed for long bone applications for over 40 years, it has only re

83 Long bones are far from being simple cylinders, so how i

84 her defects in the skull, lung, rib cage and long bones are likely to be the result of the disruption

85 and fertile, Pcolce-/- male, but not female, long bones are more massive and have altered geometries

86 number and connectivity density of SHIP(-/-) long bones are reduced, resulting in a 22% loss of bone-

87 re congenital limb malformation in which the long bones are shorter than normal, with the upper porti

88 o measure trabecular bone of limb epiphyses (long bone articular ends) in modern humans and chimpanze

89 displayed abnormalities of the thorax and/or long bones, as well as renal, hepatic, or retinal involv

90 NOER mice), cortical and trabecular bone in long bones, as well as uterus and thymus being partly de

91 ltures, and bone resorption in the fetal rat long bone assay in a dose-dependent manner.

92 e to induce bone resorption in the fetal-rat long-bone assay.

93 ar spine, and (2) focal lesions in x-rays of long bones assessed by a blinded reviewer.

94 appearance of osteoclasts from metaphyses of long bones associated with a pronounced increase in calc

95 detected DSP in the Gdm/EDTA extracts of rat long bone, at a level of about 1/400 of that in dentin.

96 In non-healing fractures of long bones, BMP signaling is severely attenuated.

97 Both mandible and long-bone BMSCs differentiated into osteoblasts.

98 ree-fold more mineralized bone compared with long-bone BMSCs.

99 is present in other mineralized tissues like long bone, calvaria, and ameloblasts.

100 of the osteogenic cells in the epiphysis of long bone carried the donor SP cell marker.

101 Histological analysis of the rib and long-bone cartilages showed a markedly diminished zone o

102 oliferating chondrocytes in developing chick long bones changes with increasing embryonic age and tha

103 from the embryonic superficial zone (eSZ) of long bones collected from late gestational murine embryo

104 biting growth retardation, shortening of the long bones, constriction of the ribcage and polydactyly.

105 tein (PTHrP)-induced resorption in fetal rat long bone cultures.

106 esis by periosteal progenitor cells within a long bone defect surrounded by periosteum and stabilized

107 d penetrance of the digit defects and causes long bone defects reminiscent of RRS, suggesting that Wn

108 including rachitic changes, hypomineralized long bones, deformations, and signs of fractures.

109 Ralpha and -beta in these processes in mouse long bone-derived osteoblastic cells and human Saos-2 ce

110 Fibroblast growth factors (FGFs) regulate long bone development by affecting the proliferation and

111 We analyzed long bone development in EGFR-deficient mice.

112 central to the coupling of angiogenesis and long bone development in mice (see the related article b

113 w the different P63 isoforms function during long bone development is largely unknown.

114 ormalities, suggesting its essential role in long bone development.

115 osine kinase that plays an important role in long bone development.

116 , perichondrium, and vascular endothelium to long bone development.

117 embers of the Wnt family, Wnt5a and Wnt5b in long bone development.

118 owth plate differentiation and thus abnormal long bone development.

119 P63 mutations suggest its essential role in long bone development.

120 It is noteworthy that long-bone development was unaffected by RCAS-dnFGFR1 inf

121 hondrocyte zone and a modest increase in the long bone diameter.

122 In long bones, diaphyseal osteoid osteomas were significant

123 erent population of BMSCs harvested from the long bone diaphysis of KO animals formed more osteoclast

124 1 (P1) observed accelerated ossification in long bone, digit and tail bones compared to their wild-t

125 elated changes in muscle and tendon lengths, long bone dimensions, and body mass.

126 r cartilage, similar to hyaline cartilage in long bones, directly transform into bone cells during en

127 olytic lesions, which develop usually in the long bones during early adulthood, show increased osteob

128 ily in the cartilaginous cores of developing long bones during embryonic and fetal development (6-13

129 Osseous abnormalities, including long-bone dysplasia with pseudarthrosis (PA), are associ

130 tumors as well as a noninvasively extendable long bone endoprosthesis.

131 mation rate (normalized to tissue volume) in long bone epiphyses, indicating that Phd2 expressed in c

132 last development in two locations in growing long bones: excavation of marrow cavities permitting hem

133 The most common primary tumor sites were the long bones (femur, tibia); the most frequent histologic

134 ochondral ossification, the process by which long bones form.

135 the growth plate cartilage, the template for long bone formation, to gain insights into this process.

136 It is associated mainly with long bone fracture and bone marrow fat passage to the sy

137 Concomitant traumatic brain injury (TBI) and long bone fracture are commonly observed in multitrauma

138 ury, followed by facial or orbital fracture, long bone fracture, and chest injury.

139 easing pain severity, and was detectable for long-bone fracture and nephrolithiasis as well as among

140 othesis, fibrin was entirely dispensable for long-bone fracture repair, as healing fractures in fibri

141 n a third of ONJ patients also suffered from long bone fractures (n = 4) and/or avascular necrosis of

142 This resulted in a two-thirds reduction in long bone fractures (P < .01), with fewer fractures per

143 n (185 733; 27%) with surgical correction of long bone fractures being the most common procedure (144

144 In patients with long bone fractures, the presence of an RLS is associate

145 s planned to qualify 50 children treated for long bones fractures of the arm, forearm, thigh and lowe

146 Orthopedic consultation should be sought for long-bone fractures, spinal cord compression, and verteb

147 Long bones from mice exposed to GC excess were collected

148 ndochondral ossification, leading to stunted long bone growth and increased pathologic neovasculariza

149 , PTHrP partially reversed the inhibition of long bone growth caused by activation of FGFR3; however,

150 drocyte maturation, leading to the nanomelic long bone growth disorder.

151 ondrocytes, which form the scaffold on which long bone growth extends, are reduced in linear dimensio

152 uretic peptide receptor B (NPR-B) stimulates long bone growth in a C-type natriuretic peptide-depende

153 We evaluated fetal long bone growth in human immunodeficiency virus (HIV)-i

154 teins caused reduced trabecular and cortical long bone growth in vivo.

155 sed a genetic mouse model to study extrinsic long bone growth modulation, in which injury is specific

156 retic peptide receptor B or NPR2, stimulates long bone growth, and missense mutations in GC-B cause d

157 tes and articular chondrocytes, not only for long bone growth, but also for bone remodeling.

158 naling affects endochondral ossification and long bone growth, causing several genetic forms of human

159 nated process of differentiation, regulating long bone growth.

160 formation reverberate on, and delay, overall long bone growth.

161 eby depleting chondrocytes needed for normal long bone growth.

162 ally leading to chondrodysplasia and reduced long bone growth.

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

164 suggested to act as a negative regulator of long-bone growth in chrondrocytes, it produces different

165 for this receptor as a negative regulator of long-bone growth.

166 l ossification in a manner similar to normal long-bone growth.

167 evelopment, and investigating the biology of long-bone growth.

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

169 Scx-mutant long bones had structural and mechanical defects.

170 ndochondral ossification in the diaphysis of long bones has been studied in-depth during fetal develo

171 MSC populations in the developing marrow of long bones have distinct functions.

172 Microarray analysis of long bones identified gene expression profiles implicati

173 e we show that MSPCs in primary spongiosa of long bone in mice at late puberty undergo normal program

174 PTH on bone formation in the mandible and a long bone in the aged ovariectomized (Ovx) rat.

175 tations in fgfr3 result in the overgrowth of long bones in a mouse model system.

176 on of mineralization, resulting in shortened long bones in adulthood.

177 ation of callus formation after fractures of long bones in children and the possibility of its altern

178 aging of callus formation after fractures of long bones in children and to analyze the correlation of

179 nent around the vertebral column, pelvis and long bones in CPDX2.

180 Vertebrae and long bones in Dmp1-deficient (Dmp1(-/-)) mice are shorte

181 y hair cells in the inner ear, and shortened long bones in the limbs.

182 uced mkp1 mRNA levels in mouse calvariae and long bones in vivo at 0.5 hours.

183 In addition, from the mutant long bones, in vitro cell cultures grown in osteogenic m

184 the hindlimb results in a shortening of the long bones, including the femur, the tibia, the fibula a

185 of osteopetrotic woven bone in the shafts of long bones into histologically normal lamellar bone.

186 imaging reveals that vessel growth in murine long bone involves the extension and anastomotic fusion

187 Shortening of the long bone is associated with a decrease in chondrocyte p

188 During limb development, the developing long bone is exposed to a concentration gradient of oxyg

189 in part, via IL-6 signaling.The strength of long bones is determined by coalescence of trabeculae du

190 induction and differentiation in developing long bones is dynamically controlled by the opposing act

191 s studies indicate that Ihh signaling in the long bones is essential for initial specification of an

192 Elongation of long bones is primarily through the growth plate, which

193 of several tissues and structures including long bones, joints and tendons, but the underlying mecha

194 tion with AC earlier in second trimester and long bones later in the second trimester.

195 omal cells (BMSCs) differs between MB versus long bones (LB).

196 Long bone length in dogs is a unique example of multiple

197 association between placental VDR and fetal long bone length may indicate a role for VDR in fetal bo

198 y craniofacial dysplasia, scapula dysplasia, long bone length shortage and body weight decrease compa

199 wder diet group featured normal body weight, long bone length, and serum alkaline phosphatase activit

200 by widening of the metaphyses, reduction of long bone length, and short stature.

201 outcomes were examined in relation to fetal long bone length, placental VDR, serum 25-hydroxyvitamin

202 h is a cartilaginous structure at the end of long bones made up of chondrocytes.

203 no growth retardation, and their facial and long bones maintained the normal size and shape.

204 f mesenchymal stem cells (MSCs) derived from long bone marrow (BMMSCs), mouse MSCs derived from orofa

205 but decreased mineral deposition by Enpp1-/- long bone marrow-derived osteoblasts in comparison to wi

206 established a protocol for rat mandible and long-bone marrow stromal cell (BMSC) isolation and cultu

207 Here, we hypothesized that rat mandible vs. long-bone marrow-derived cells possess different osteoge

208 reased serum osteocalcin levels and improved long bone mass and microarchitecture in SAMP-6 senescent

209 ovitaminosis D) causes osteomalacia and poor long bone mineralization.

210 terized by fetal akinesia, shortening of all long bones, multiple contractures, rib anomalies, thorac

211 acterized by micromelia with broad and bowed long bones, narrow thorax and craniofacial abnormalities

212 uce new bone formation in spinal fusions and long bone non-union fractures.

213 s junction and the metaphyseal periosteum of long bones, nor were they present in tooth eruption path

214 ls are concentrated within the metaphysis of long bones not in the perisinusoidal space and are neede

215 ossess the wide body, long pubis, and robust long bones of adult Neandertals.

216 in the mid-region of the growth plate in the long bones of all NOMID mice that may be the precursor t

217 ased cell migration in vivo, we analyzed the long bones of c-Cbl(-/-) mice during development.

218 This study showed that the long bones of cKO mice were shorter and had a lower leve

219 ivo, we have analyzed the bone collar in the long bones of embryos in which Ihh was artificially expr

220 ice and the hypomineralized phenotype of the long bones of Enpp1-/- mice are not rescued by simultane

221 The long bones of mutant mice contain thinner cortical bone

222 Osteoclasts were isolated from long bones of neonatal rats and rabbits.

223 w that cortical growth marks are frequent in long bones of New Zealand's moa (Aves: Dinornithiformes)

224 d mineralization density was observed in the long bones of older animals which showed modelling defor

225 anical strain was increased and decreased in long bones of ovariectomized rats by treadmill exercise

226 However, we observed a phenotype in the long bones of Prkca(-/-) female but not male mice, in wh

227 Importantly, long bones of Prx1-Cre;KL(fl/fl) mice but not their axia

228 We searched ca. 70-year-old long bones of putative Finnish casualties from World War

229 Long bones of the appendicular skeleton are formed from

230 more additional fractures that involved the long bones of the upper and lower extremities, and seven

231 The long bones of the vertebrate appendicular skeleton arise

232 h) signaling is significantly reduced in the long bones of these embryos.

233 mad1 and Runx2 protein similarly to those in long bones of TNF-Tg mice.

234 EPCs were isolated from the long bones of Wistar rat bone marrow.

235 ramembranous bone formation in the shafts of long bones, only the PTH/PTHrP-R(-/-) bones exhibit a st

236 eoclasts and decreased 45Ca release in fetal long-bone organ cultures.

237 ondylar ramus (1 ossification center) versus long bone ossification formation (2 ossification centers

238 r growth derived by a developmental study of long bone ossification in the mutants.

239 steocyte processes vs. cell bodies in murine long bone osteocyte Y4 (MLO-Y4) cells with physiological

240 2), diabetic pedal osteomyelitis (n = 8), or long bone osteomyelitis (n = 4) were imaged 5, 30, 60, a

241 Their long bone osteopetrosis is largely reversed, and extensi

242 In humans, mutations in fibrillins result in long bone overgrowth as well as other distinct phenotype

243 neurysm, dislocation of the ocular lens, and long-bone overgrowth.

244 h shown to mitigate both the chondrocyte and long-bone pathology of PSACH in a mouse model and sugges

245 ion of Scx during development led to altered long bone properties and callus healing.

246 Using diaphyseal long bone radial defects in a diabetic rabbit model it w

247 ertrophic at the periphery of the developing long bones rather than in the middle, leading to a seemi

248 ALK5(CKO) mice had short and wide long bones, reduced bone collars, and trabecular bones.

249 uced a loss of skeletal integrity leading to long bone regression and loss of skeletal turnover.

250 Klotho expression in long bones regulates FGF23 production during renal failu

251 Proper longitudinal growth of long bones relies on the regulation of specific spatial

252 its enzymatic activity did not affect normal long bone remodeling.

253 ous Fgf-9 seems to play an important role in long bone repair.

254 this study, we analyzed the role of Fgf-9 in long bone repair.

255 Formation of the long bones requires a cartilage template.

256 significant bone resorption in the fetal rat long bone resorption assay when compared with untreated

257 Histological analysis of the long bones revealed that the growth plate contained smal

258 rays, we followed gene expression changes in long bone RNA when CSF-1 injections were used to restore

259 Long-bone RNA from CSF-1-treated tl/tl rats was analyzed

260 sed in many mammalian tissues, including the long bone's growth plate.

261 Osteoblasts derived from bone marrow or long bone samples of adult tumor necrosis factor (TNF) t

262 33,536, which has the ability to heal canine long bone segmental and fracture model defects without t

263 Bone erosion was particularly evident in long bone shafts, progressively increased from Binet sta

264 he geometric and biomechanical properties of long bones show increases in the moments of inertia, end

265 ereas Ppia(-/-) osteoclasts derived from the long bones showed increased osteoclastic activity.

266 resulting in growth defects of the skull and long bones, showed that these enhancers function in an a

267 in breast, prostate, or lung metastasize to long bones, spinal vertebrae, and/or pelvis.

268 during chondrogenesis in a developing human long bone (stage XXI).

269 Long bone strength is determined by its outer shell (cor

270 However, very recent studies in long bone suggest that chondrocytes can directly transfo

271 erentiation were not altered in vertebrae or long bones suggesting that loss of responsiveness to TGF

272 y cultures of the lung, calvaria, cartilage, long bone, tail, and skin.

273 The long bones that develop in the absence of wild-type Disp

274 In developing long bones, the growing cartilage and bone are surrounde

275 In the long bones, the growth plates (GPs) drive elongation by

276 rated that, in contrast to the vertebrae and long bones, the sternum of wild-type embryos expresses h

277 e hypertrophic are located in the centers of long bones; this polarity is greatly diminished in both

278 ugh endochondral ossification, the growth of long bones through proliferation and differentiation of

279 Rather, microscopic analyses of the long-bone tissues show that dinosaurs grew to their adul

280 lts demonstrate the pivotal role of PTH1R in long bones to regulate systemic mineral ion homeostasis

281 arily characterized by short ribs, shortened long bones, varying types of polydactyly and concomitant

282 Here we show that the long bone vasculature generates a peculiar flow pattern,

283 rocytes of the endochondral craniofacial and long bones, vertebrae and ribs.

284 n total density and in cortical thickness of long bones was documented by histology and quantitative

285 Alteration in the length of the long bones was primarily due to a decrease in chondrocyt

286 restingly, overall growth and lengthening of long bones were also delayed in the mutants.

287 st numbers in the inflamed joints and in the long bones were compared.

288 cell suspensions from the red marrow of the long bones were cultured 14 days in vitro and subsequent

289 alterations in length and mineralization of long bones were not detected at E17.5 days.

290 then killed and bone marrow plasma from the long bones were obtained, concentrated, and assayed for

291 eletal phenotype of that of the Vhl mutants: long bones were significantly thinner and less vasculari

292 mals generated by this means develop shorter long bones when compared to wild-type littermates.

293 contrast to the initial ossification site in long bone, which is in the center.

294 radiographic evidence of at least one mature long bone who were at least 12 years old and weighed at

295 bnormalities including shorter, more slender long bones with decreased mechanical strength as well as

296 There were no stress fractures of long bones with prolonged therapy.

297 is of the skull and abnormal modeling of the long bones, with little or no joint pathology.

298 een and marked infiltration in vertebrae and long bones, with loss of bony trabeculae and increased O

299 l thickening, mainly in the diaphysis of the long bones, without extensive periosteal reaction or sof

300 Long-bone x-rays showed no change in focal lesions or bo