ライフサイエンスコーパス: bone

1 and one with a stress fracture of the sacral bone.

2 ed anti-valgus osteotomy of the right tibial bone.

3 air, inner air, soft tissue, and continuous bone.

4 ous bridging and/or clefting with the parent bone.

5 atory drugs frequently do not repair damaged bone.

6 erating a scaffold progressively replaced by bone.

7 r spacing, but it simultaneously damaged the bone.

8 omic location that is frequently adjacent to bone.

9 ession in joints versus growing ends of long bones.

10 ascals [MPa]) promoting crack propagation in bones, (2) tooth form and dental arcade configurations t

11 olume, but not with the severity of brain or bone abnormalities.

12 o compare the performance of a deep-learning bone age assessment model based on hand radiographs with

13 ization is a key process in the formation of bone and cartilage in vertebrates, involving the deposit

14 peripheral nervous system, melanocytes, and bone and cartilage of the face.

15 vity, and osteotomy site healing in type III bone and high endogenous Wnt signaling.

16 in their detection ability, particularly of bone and liver micrometastases.

17 ibiotics significantly improved the alveolar bone and PDL damage of the knockdown phenotype, which ar

18 Natural structural materials like bone and shell have complex, hierarchical architectures

19 his systematic review is to examine marginal bone and soft tissue level changes, technical and biolog

20 ry may result in irrigant extrusion into the bone and soft tissues surrounding the tooth.

21 (with the exception of the missing occipital bone) and a fragmentary right maxilla preserving part of

22 al role in the maintenance and repair of our bones are formed from bone marrow myeloid progenitor cel

23 periodontal augmentation (soft tissue and/or bone augmentation) therapies for patients undergoing ort

24 NKA infection compared to those receiving KO bone barrow (P < 0.001).

25 eared all tested organs, including calcified bone, but the fluorescence of proteins and immunohistoch

26 We hypothesized that Klotho in bone cells is part of an autocrine feedback loop that re

27 dies offer a glimpse into how these critical bone cells respond to mechanical load in vivo, as well a

28 rs, C5aR1 and C5aR2, expressed on immune and bone cells.

29 kin-6 significantly correlated with alveolar bone changes (P <0.05), whereas adipsin showed a negativ

30 OCS3-dependent cytokine expression regulates bone corticalization.

31 ractory multiple myeloma because it assesses bone damage with relatively high sensitivity and specifi

32 rib with adjacent muscle and skin to restore bone defects, internal lining, and external coverage.

33 ns (ACP) recommendations on treatment of low bone density and osteoporosis to prevent fractures in me

34 ic conditions, thus implicating FGF23 in low bone density in cetaceans.

35 ate FRAX scores using data from the Manitoba Bone Density Program database of all women and men 40 ye

36 Condensation increased interfacial bone density, as measured by a significant change in bon

37 ion of FGF23, a gene associated with reduced bone density, is greatly increased in the cetacean liver

38 n patterning the stapes and incus middle ear bones derived from the equivalent pharyngeal arches of m

39 Circulating levels of bone-derived fibroblast growth factor 23 (FGF23) increas

40 al cavity and to prevent subsequent alveolar bone destruction and osteoclastogenesis.

41 cted to identify the role of Scx in cortical bone development and fracture healing.

42 we show here plays no apparent role in early bone development and homeostasis, but which is required

43 r arch identity, thus ensuring separation of bone development between the upper and lower jaws.

44 ant human disorder characterized by abnormal bone development that is mainly due to defective intrame

45 rteriosclerosis, vascular calcification, and bone disorders, all of which are also associated with ag

46 play a pivotal role in diagnosing metabolic bone disorders.

47 ction in the growth plate, which counteracts bone elongation.

48 ony callus formed between allograft and host bone ends in both young P3 MSC and aged P10 MSC sheet-wr

49 Bone erosion was particularly evident in long bone shaft

50 Stimulation of normal-weight bone explant with recombinant resistin increased the Typ

51 membrane exposure and a noteworthy, ectopic bone formation above the mesh in 72% of sites.

52 ymal progenitors responsible for both normal bone formation and fracture repair.

53 de of type I collagen (CTX-I) are markers of bone formation and resorption, respectively, that are re

54 tion of beta-catenin significantly increased bone formation and slightly hindered bone resorption.

55 p38alpha ablation resulted in a decrease in bone formation and the number of bone marrow mesenchymal

56 t1 overexpression from osteocytes stimulated bone formation by increasing osteoblast number and activ

57 t is mainly due to defective intramembranous bone formation by osteoblasts.

58 also enhances osteoblast differentiation and bone formation from mesenchymal stem cells.

59 nstrating no significant difference in vital bone formation or dimensional changes among 50%/50% cort

60 e concluded that the material resorption and bone formation was highly impacted by the particle-speci

61 The nHA-LC (38% HA content) paste supported bone formation with a high defect bridging-rate.

62 or without rMSC aggregates resulted in less bone formation, indicating a prominent role of DA in eff

63 the rate of bone resorption exceeds that of bone formation, so we investigated the role of the osteo

64 s underlying the role of FCSCs in regulating bone formation.

65 eocyte-specific Wnt antagonist that inhibits bone formation.

66 maintained by balancing OC function with the bone-forming function of osteoblasts.

67 th seven affected members exhibited frequent bone fractures and florid osseous dysplasia (p.Cys356Tyr

68 Sclerostin was expressed in osteocytes from bones from naive and myeloma-bearing mice.

69 We aimed to characterize early changes in bone functional properties in critical illness and their

70 the dairy equivalent is adequate for normal bone gain between ages 8 and 16 y.

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

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

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

74 vating mutations in the FGF receptor inhibit bone growth.

75 ondral ossification in the diaphysis of long bones has been studied in-depth during fetal development

76 osseointegration to determine if one type of bone healed faster and supported osseointegration better

77 adipocytic lineage inhibit hematopoiesis and bone healing, potentially by producing excessive amounts

78 osteoblasts and osteoclasts is required for bone health and homeostasis.

79 dose effect of vitamin D supplementation on bone health and suggest that race/ethnicity and BMI play

80 and BMI play an important role in pregnancy bone health.

81 significant difference in residual alveolar bone height (P <0.001).

82 This research represents the only bone histology analysis of the dodo and provides an unpr

83 Proper bone homeostasis and skeletal strength are maintained by

84 rine peptide hormones involved in control of bone homeostasis, glucose regulation, satiety, and gastr

85 computation method based on segmentation of bones in CT and of lesions in PET.

86 55 patients with biopsy-proven SUSCC without bone invasion treated by wide surgical excision of the n

87 Infection of bone is a severe complication due to the variety of bact

88 A significant proportion of bone is accrued after adult height is achieved.

89 Long bone length in dogs is a unique example of multiple dise

90 A high correlation between bone lesion quantity as determined visually and automati

91 The primary end point was the detection of bone lesions at diagnosis by MRI versus PET-CT.

92 f apico-coronal implant placement on crestal bone levels.

93 and probing depth [PD] >/=4 mm) and crestal bone loss (CBL) around immediately loaded (IL) and delay

94 equired for osteoclast-mediated inflammatory bone loss and hyper-multinucleation of OCs.

95 Our findings indicate that CLP causes bone loss by enhancing Itch-mediated osteoclastogenesis,

96 ll transfer demonstrated reduced periodontal bone loss compared to the no-transfer group and the grou

97 genesis, and protects mice from pathological bone loss in disease models.

98 ts enhancing osteoclastogenesis, which drive bone loss in health.

99 L), which, in turn, promotes the periodontal bone loss via upregulation of osteoclastogenesis.

100 of remaining teeth, percentage of teeth with bone loss, implant function time, implant surface, and p

101 Postextraction alveolar bone loss, mostly affecting the buccal plate, occurs des

102 ks experimental periodontal inflammation and bone loss, suggesting a promising platform for the devel

103 c and prosthetic complications, and marginal bone loss.

104 +)-dependent mechanisms causing pathological bone loss.

105 nds and/or paracrine Wnts emanating from the bone marrow (BM) niche.

106 ells (HSCs) are mobilized from niches in the bone marrow (BM) to the blood circulation by the cytokin

107 optimal compared with that seen in wild-type bone marrow (BM)-transplanted OS mice in peripheral bloo

108 lophosphamide was originally described using bone marrow (BM).

109 demonstrated increased [(18)F]-FDG uptake in bone marrow 4 days postinfection compared to surviving N

110 The ratio of mean tumor to bone marrow absorbed dose per unit administered activity

111 e aging characteristics, including increased bone marrow adiposity, decreased bone mass, and impaired

112 Meanwhile, it also inhibited bone marrow adiposity.

113 matched unrelated (MUD) donor T-cell-replete bone marrow allografting, obviating the need for additio

114 lls promoted tumor cell dissemination in the bone marrow and enhanced osteolytic lesion formation, ir

115 In contrast, the bone marrow and lymph nodes of nonsurvivors showed incre

116 We assessed differentiation of B cells in bone marrow and spleen and analyzed their endosomal morp

117 semination of colorectal cancer cells in the bone marrow and tumor-driven osteolytic lesion formation

118 Bone marrow aspiration from the iliac crests and in vivo

119 odies (n = 163) for the presence of abnormal bone marrow attenuation on VNCa images by using color-co

120 more efficiently reduce the clonogenicity of bone marrow cancer cells from patients with acute myeloi

121 ine effects of transplanted unmodified human bone marrow CD34+ (hBM34+) cells into symptomatic G93A m

122 receptor family, is expressed in myeloid and bone marrow cells and was implicated as a checkpoint reg

123 ice were irradiated and given transplants of bone marrow cells from C57BL6 mice, with or without the

124 ent feedback mechanism through which myeloid bone marrow cells restore quiescence of myeloid-biased H

125 Consistent with this, bone marrow chimera studies show that aberrant Pkhd1 mus

126 g homeostasis, gammadeltaT17 cells emerge in bone marrow chimeric mice upon induction of skin inflamm

127 Using mixed bone marrow chimeric mice, we show that the impact of NK

128 REAM KO control mice, but not in WT or DREAM bone marrow chimeric mice.

129 enhanced maturation and cytokine release of bone marrow dendritic cells in vitro.

130 both local expansion of metabolically active bone marrow documented by FDG uptake and with the number

131 Additionally, jagged-2 expressed in bone marrow ECs regulated HSPC cell cycle and quiescence

132 This defect was rescued by bone marrow exosomes from WT, but not miR-155(-/-), cell

133 cause of the short half-lives and suboptimal bone marrow exposure of the drugs.

134 dult mice resulted in acute lethality due to bone marrow failure and intestinal atrophy featuring ste

135 or older with thrombocytopenia secondary to bone marrow failure, requiring prophylactic platelet tra

136 plasma cells (LLPCs), which persisted in the bone marrow for several months after vaccination.

137 ion, LOX was expressed by tumor cells in the bone marrow from colorectal cancer patients with bone me

138 GSNOR KO animals receiving WT bone marrow had significantly reduced survival following

139 s blood parameters, leukocyte depletion, and bone marrow hypoplasia.

140 Increased bone marrow hypoxia is associated with increased recircu

141 inducible NPs containing RA can engraft into bone marrow in vivo in the proximity of other leukaemic

142 Furthermore, transplantation of WT bone marrow into miR-155KO mice mitigated this phenotype

143 re of epicardial origin and not derived from bone marrow lineages, endothelial-to-mesenchymal transit

144 e 1 (ENPP1) is preferentially upregulated in bone marrow LLPCs compared with their splenic short-live

145 decrease in bone formation and the number of bone marrow mesenchymal stem/stromal cells, likely due t

146 acebo-controlled trial comparing 150 million bone marrow mononuclear cells versus placebo in 120 pati

147 The test group received allogeneic bone marrow MSCs by intradiscal injection of 25 x 10 cel

148 Conditional depletion of Foxp1 in bone marrow MSCs led to premature aging characteristics,

149 In bone marrow MSCs, FOXP1 expression levels declined with

150 ance and repair of our bones are formed from bone marrow myeloid progenitor cells by a complex differ

151 llenge, the clonal response of leukocytes in bone marrow of acute myeloid leukaemia (AML) patients, a

152 in vivo and were detectable in the blood and bone marrow of patients who had a response and patients

153 Bone marrow reconstitutions showed that a lncRNA express

154 In bone marrow samples, the microfluidic-based plasma cell

155 ogressively impairs their homeostasis in the bone marrow through an unidentified mechanism.

156 and Functional Assessment of Cancer Therapy-Bone Marrow Transplant.

157 The combination of bone marrow transplantation and local muscle radiation p

158 Bone marrow transplantation failed to rescue outgrowth.

159 , dermatologic conditions, or solid-organ or bone marrow transplantation.

160 sident beds that could not be transferred by bone marrow transplantation.

161 y and resident monocytes are retained in the bone marrow vasculature, representing an important reser

162 d dose per unit administered activity to the bone marrow was 0.13, 0.086, 0.33, and 0.068 mGy/MBq aft

163 Surprisingly, the collapse of the Rev1Xpc bone marrow was associated with progressive mitochondria

164 The tumor-to-dose-limiting-organ (bone marrow) absorbed dose ratio, that is, the therapeut

165 ssue (cholangiocytes) and the immune system (bone marrow).

166 ve sampling from ileum, rectum, lymph nodes, bone marrow, CSF, circulating CD4+ T cell subsets, and p

167 the presence of cytokeratin(+) cells in the bone marrow, this MSC subpopulation could prove useful i

168 Monocytes can mobilize from bone marrow, traffic to their required destination, and

169 is critical for protection from IRI through bone marrow-derived adenosine 2a receptors.

170 hat PGE2 inhibits IL-27 production in murine bone marrow-derived DCs.

171 lations of wild-type mice with Nrp1-depleted bone marrow-derived macrophages (BMDM) confers resistanc

172 eficient RAW cells and primary PHD2 knockout bone marrow-derived macrophages (BMDM).

173 aB pathway (IKKalpha/beta, NF-kappaB p65) in bone marrow-derived macrophages (BMDMs) from knockout mi

174 The effects of estrogen are long-lasting; bone marrow-derived macrophages from ovariectomized mice

175 CD44(+/+) murine bone marrow-derived macrophages produced higher TNF-alph

176 oxide addition to CB3-infected NOD.Ncf1(m1J) bone marrow-derived macrophages rescued the inflammatory

177 In SIRT3 knock-out bone marrow-derived macrophages, NLRP3 activation promot

178 We have found that in murine bone marrow-derived macrophages, PGE2 via the cAMP/prote

179 Hierarchical clustering demonstrated that bone marrow-derived mast cells and BMBs shared specific

180 UC-MSCs in vitro, compared with bone marrow-derived mesenchymal stem cells, displayed a

181 nce its down-regulation (DR) in both ex vivo bone marrow-derived mesenchymal stromal cells (MSC) and

182 were then used for the batch transduction of bone marrow-derived mesenchymal stromal cells ex vivo, f

183 eared from the serum by liver-, spleen-, and bone marrow-resident phagocytic cells.

184 ading to ectopic platelet release within the bone marrow.

185 ery limited ability to repopulate from donor bone marrow.

186 of essential phenomena occurring within the bone marrow.

187 lenge mobilized ILC2 progenitors to exit the bone marrow.

188 chymal stromal cells and cancer cells in the bone marrow.

189 ressor cells (MDSC) from precursors in mouse bone marrow.

190 r in the presence of cytokeratin(+) cells in bone marrow.

191 ABIN1[D485N] mice transplanted with WT mouse bone marrow.

192 ranscriptome and cytometry analyses in mixed bone-marrow (BM) chimeras.

193 dalar activity was associated with increased bone-marrow activity (r=0.47; p<0.0001), arterial inflam

194 T imaging objectively identified subclinical bone-marrow recovery within 5 days of HSC infusion, whic

195 d quantification and tracking of subclinical bone-marrow repopulation in human beings and revealed ne

196 lic variations are associated with decreased bone mass and osteoporosis in humans.

197 g increased bone marrow adiposity, decreased bone mass, and impaired MSC self-renewal capacity in mic

198 ncreased risk of osteosarcoma, and decreased bone mass.

199 inflammasomes, we tested the hypothesis that bone matrix components function as DAMPs for the NLRP3 i

200 sue and the vasculature within the calcified bone matrix.

201 results reveal a novel role for Erk5 during bone maturation and homeostasis in vivo.

202 nevertheless functions atypically to support bone maturation.

203 rated specific localization to breast cancer bone metastases in mice.

204 hted imaging (DWI) to assess the response of bone metastases to treatment in patients with metastatic

205 quences for the detection of probable spinal bone metastases, thereby providing an opportunity to red

206 ials of BMAs in control of pain secondary to bone metastases.

207 marrow from colorectal cancer patients with bone metastases.

208 review, we evaluate the importance of ERs in bone metastasis and discuss new avenues of investigation

209 or the necessity for radiation or surgery to bone metastasis cause considerable morbidity, decrements

210 ight offer a new possibility for diminishing bone metastasis formation.Significance: These findings e

211 Bone metastasis is a prominent cause of morbidity and mo

212 and discuss new avenues of investigation for bone metastasis treatment based on current knowledge.

213 tic agent for the prevention or treatment of bone metastasis.

214 ease bone stromal activity in the absence of bone metastasis.

215 We find that several fossilizable aspects of bone microstructure, including the sizes of vascular and

216 Little is known about bone mineral density (BMD) during pregnancy.

217 e-wide association study summary datasets of bone mineral density (BMD).

218 g from autism have been reported to have low bone mineral density and increased risk for fracture, ye

219 genetic factors with pleiotropic effects on bone mineral density and lean mass.Bone mineral density

220 ffects on bone mineral density and lean mass.Bone mineral density and lean skeletal mass are heritabl

221 In this population-based cohort study, bone mineral density and risk factors were used to calcu

222 uce fragility fractures in patients with low bone mineral density is beyond the scope of the guidelin

223 ice by adoptive transfer, and bone turnover, bone mineral density, and indices of bone structure and

224 ect to their metabolic bone status including bone mineral density, calcium kinetics studies, and mark

225 users should not routinely screen or monitor bone mineral density, serum creatinine, magnesium, or vi

226 The Bone Morphogenetic Protein (BMP) family reiteratively si

227 red neogenic hair follicles, which triggered bone morphogenetic protein (BMP) signaling and then acti

228 rates that RNAi silencing of a member of the Bone Morphogenetic Protein (BMP) signaling pathway, Deca

229 f these mutants target the components of the Bone Morphogenetic Protein (BMP) signaling pathway, reve

230 wingless-related integration site (WNT), and bone morphogenetic protein (BMP) signalling interactions

231 pression and signaling are up-regulated, and bone morphogenetic protein (BMP) signals are impaired.

232 teogenic transcription factors in normal jaw bone MSCs.

233 pired by the highly ordered nanostructure of bone, nanodopant composite biomaterials are gaining spec

234 tivation, osteoblast metabolic activity, and bone nodule formation.

235 Uterine neoplasms, myometria and jaw bones of Cdc73(+/-) mice had increased proliferation rat

236 well-defined mechanical loads to metatarsal bones of living mice while simultaneously monitoring the

237 s among groups regarding percentage of vital bone or CT/other.

238 tribute to sensory nerves that innervate the bone or skeletal tissue has not been shown.

239 ar ramus (1 ossification center) versus long bone ossification formation (2 ossification centers).

240 derived from human MT in the pathogenesis of bone outgrowth.

241 and buccal depth of space between tooth and bone, periosteal reaction, serpentine bone resorption, a

242 for fracture, yet the cellular origin of the bone phenotype remains unknown.

243 Taphonomic processes affecting bone post mortem are important in forensic, archaeologic

244 We show that bone pulverization was made possible through a combinati

245 The fundamental question of how bone quality is affected in AIS remains controversy beca

246 recurrent nodules, maximum recurrence size, bone recurrence, alphafetoprotein at recurrence, donor s

247 GF-2) could be an effective way of promoting bone regeneration in patients with diabetes.

248 For in vivo bone regeneration, HCCS-PDA or HCCS particulates with or

249 mation, the recruitment of immune cells, and bone regeneration, resulting in delayed fracture healing

250 dicating a prominent role of DA in effective bone regeneration.

251 ite-matched control for detailed analysis on bone-related parameters.

252 Here, we report that ancient fish-bone remains, despite being porous, brittle, and light,

253 ry cytokines, including TNF, interferes with bone remodeling during inflammation through Ca(2+)-depen

254 vealed a strong positive correlation between bone remodeling rates, mitotic activity, and osteotomy s

255 ty, calcium kinetics studies, and markers of bone remodeling.

256 not only for long bone growth, but also for bone remodeling.

257 Their slender distal limb bones resemble those of Asiatic asses, such as the Persi

258 Conversely, bone-resident cells committed to the adipocytic lineage

259 Bone-resorbing multinucleated osteoclasts that play a ce

260 Osteopenia occurs where the rate of bone resorption exceeds that of bone formation, so we in

261 th and bone, periosteal reaction, serpentine bone resorption, abscess formation, and root penetration

262 creased bone formation and slightly hindered bone resorption.

263 bone turnover markers for assessment of the bone safety of new medications.

264 We additionally dated animal bone samples from units G1 and G1-G3 These dates suggest

265 In 31 patients, bone scanning and radiologic imaging were performed for

266 s than 10% of the price for plastic embedded bone sections.

267 one erosion was particularly evident in long bone shafts, progressively increased from Binet stage A

268 BPS804 treatment increased mean ALP and bone-specific ALP enzymatic activity between days 2 and

269 oarray (TMA) analysis to a sample of femoral bone specimens from 20 exhumed individuals of known peri

270 als with RTS with respect to their metabolic bone status including bone mineral density, calcium kine

271 We tested the bone status of long-term KTR using all 3 techniques.

272 (n = 70) that lung adenocarcinomas increase bone stromal activity in the absence of bone metastasis.

273 rnover, bone mineral density, and indices of bone structure and turnover were quantified.

274 pplied research on the correlated changes in bone structure, brain size and the many other affected o

275 illness and their relationship to changes in bone structure, using a sepsis rodent model.

276 scess formation, and root penetration of the bone surface and analyzed by analysis of variance.

277 ence staining on multinucleated cells at the bone surface of inflamed mouse joints.

278 s in the liver, lung, pancreas, kidneys, and bone, that have disseminated from the primary site, are

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

280 pid, simultaneous visualisation of calcified bone tissue and the vasculature within the calcified bon

281 hymal stromal cells (MSCs) could be used for bone tissue regeneration as tissue engineered periosteum

282 special attention for their ability to guide bone tissue regeneration through structural and biologic

283 clinical outcomes in the surgical removal of bone tumor.

284 in a subset of 553 patients, suppression of bone turnover (assessed by C-terminal telopeptide levels

285 o interactions were observed between lead or bone turnover and other prognostic indicators.

286 Here, we investigated bone turnover and regeneration in mice lacking either C5

287 studies are needed to investigate the use of bone turnover markers for assessment of the bone safety

288 beta knockout mice by adoptive transfer, and bone turnover, bone mineral density, and indices of bone

289 loss caused by estrogen deficiency, improved bone turnover, promoted a favorable estrogen metabolite

290 ey atrophy, hyperphosphatemia, and increased bone turnover.

291 Gradual bone uptake was, however, also observed.

292 3D imaging of the bone vasculature is of key importance in the understandi

293 ablated in osteocytes, have high trabecular bone volume and poorly defined metaphyseal cortices.

294 no significant correlation between alveolar bone volume changes and increased BW or glucose toleranc

295 wed that I-PTH treatment led to an increased bone volume fraction, tissue density and trabecular thic

296 ow that in addition to dramatic increases in bone volume, Sost(-/-) mice exhibit a reduction in adipo

297 and microcomputed tomography examination of bone volume/levels.

298 sity, as measured by a significant change in bone volume/total volume and trabecular spacing, but it

299 the role of I-PTH on the MCC and subchondral bone, we carried out our studies using 4 to 5 week old t

300 d fibrin-encapsulated abscess communities in bone were also increased, further linking fibrin deposit