ライフサイエンスコーパス: bone mass

1 recognized window of opportunity to optimize bone mass.

2 hat regulates osteoclast multinucleation and bone mass.

3 of activin receptor signaling in regulating bone mass.

4 rotein that is mutated in patients with high bone mass.

5 animals causes a 50% decrease in trabecular bone mass.

6 itor YKL-05-099 increases bone formation and bone mass.

7 of offspring at 4 mo of age, the age of peak bone mass.

8 nervous system activation leads to decreased bone mass.

9 ded markedly reduced trabecular and cortical bone mass.

10 ns in WBB6F1/J-Kit(W/W-v) mice result in low bone mass.

11 cally in postnatal mice increased trabecular bone mass.

12 T16 surprisingly increases mainly trabecular bone mass.

13 e associations between dietary acid load and bone mass.

14 e, and Wnt16(-/-) mice have reduced cortical bone mass.

15 teocyte viability to strength independent of bone mass.

16 s to bone repair and maintenance of cortical bone mass.

17 spaceflight are loss of skeletal muscle and bone mass.

18 rder characterized by bone fragility and low bone mass.

19 efore, contribute to the age-related loss of bone mass.

20 exhibit elevated bone resorption and reduced bone mass.

21 PTH to stimulate bone formation and increase bone mass.

22 f osteoclastogenesis, resulting in increased bone mass.

23 and suggests potential therapies to increase bone mass.

24 oblasts, impaired mineralization and reduced bone mass.

25 ssue characterized by bone fragility and low bone mass.

26 eoclastic bone resorption to maintain normal bone mass.

27 JDP2(-/-) mice were found to have increased bone mass.

28 ice exhibit lower bone resorption and higher bone mass.

29 -VCL and LysM-VCL mice exhibit a doubling of bone mass.

30 al inactivity are both associated with lower bone mass.

31 etary intake during pregnancy with childhood bone mass.

32 tes did not influence cancellous or cortical bone mass.

33 ed the hypothesis that Pb negatively affects bone mass.

34 eful therapeutic targets for upregulation of bone mass.

35 calcium intake may adversely affect maternal bone mass.

36 ntrations were not associated with childhood bone mass.

37 C (PKC) and other proteins in the control of bone mass.

38 e-mediated degradation and thereby increases bone mass.

39 ion leads to a bone fragility independent of bone mass.

40 s increases their numbers, but also enhances bone mass.

41 m inhibition of shn3 in adult mice increases bone mass.

42 od and current therapies do not restore lost bone mass.

43 ral density in postmenopausal women with low bone mass.

44 n ISS (international space station) on mouse bone mass.

45 ncreased risk of osteosarcoma, and decreased bone mass.

46 e a potential therapeutic target to increase bone mass.

47 e tissue (MAT) is negatively associated with bone mass.

48 how fewer CD31(hi)Emcn(hi) vessels and lower bone mass.

49 eoclastogenic deficit and reduces trabecular bone mass.

50 e young mutant mice showed minor increase in bone mass, 6-month-old mutant mice developed osteoporosi

51 mice completely lacking LRP6), we infer that bone mass accrual and dental patterning are more sensiti

52 ndicate that Rhbdf2 plays a decisive role in bone mass accrual and microarchitecture.

53 on and urbanized lifestyles in later life on bone mass accrual in young adults from a rural community

54 Because bone mass accrual is completed by young adulthood, asses

55 ed factors contribute to lifelong growth and bone mass accrual, although the specific role of materna

56 cued the defects in replication capacity and bone mass accrual.

57 dolescence, which is a period of substantial bone mass accrual.

58 ant environmental factor that influence both bone mass accumulation during childhood and adolescence

59 Sex steroids are critical for peak bone mass acquisition in both genders.

60 Stimulant use was associated with lower bone mass after adjustment for covariates.

61 rations were associated with lower childhood bone mass (all P-trend < 0.01).

62 bones, and prevent attainment of a high peak bone mass, all of which will increase susceptibility to

63 ay impair bone accrual in childhood and peak bone mass, an important determinant of lifelong skeletal

64 alcium intake results in higher lumbar spine bone mass and a reduced rate of femoral neck bone loss d

65 Food intake, muscle and bone mass and adiposity were unchanged in Sgta(-/-).

66 ld type (wt), db mice displayed reduced peak bone mass and age-related trabecular and cortical bone l

67 Low bone mass and an increased risk of fracture are predicto

68 mouse model] reduced cortical and trabecular bone mass and attenuated PTH-induced trabecular bone ana

69 f Phd2 in chondrocytes resulted in increased bone mass and bone formation rate (normalized to tissue

70 However, their effects on bone mass and bone metastasis are unknown.

71 We show that bone mass and bone production and resorption, as well as

72 of beta-catenin significantly increased the bone mass and delayed the bone remodeling process, resul

73 from B cells did not alter B cell number or bone mass and did not alter the response to ovariectomy.

74 body (Scl-Ab) treatment effectively improved bone mass and dramatically decreased fracture rate in sw

75 , improved bone microarchitecture, increased bone mass and enhanced mechanical properties in both ost

76 classic signs of osteopetrosis such as high bone mass and failure of tooth eruption.

77 Stimulating bone formation to increase bone mass and fracture resistance is a priority; however

78 ibody and zoledronic acid combined increased bone mass and fracture resistance when compared with tre

79 tg7 in the entire osteoblast lineage had low bone mass and fractures associated with reduced numbers

80 thelium-derived factor restoration increases bone mass and improves bone plasticity in a model of ost

81 CR mice had low bone mass and increased BMAT in the proximal tibias.

82 y predominates, resulting in equalization of bone mass and increased longitudinal and radial bone gro

83 e effect was found with increased trabecular bone mass and increased PTH-induced anabolism.

84 esulting in alterations of linear growth and bone mass and increased risk for osteoporosis and pathol

85 Glucocorticoid (GC) therapy decreases bone mass and increases the risk of fractures.

86 chloride transport in osteoblasts normalizes bone mass and microarchitecture in murine CF.

87 d serum osteocalcin levels and improved long bone mass and microarchitecture in SAMP-6 senescent oste

88 ell adhesion, which could be used to improve bone mass and microarchitecture in the aging skeleton.

89 (120 mg/kg once a day for 28 days) improved bone mass and microarchitecture in the lumbar spine and

90 ntinued throwing during aging, some cortical bone mass and more strength benefits of the physical act

91 Phlpp1 null mice exhibit decreased bone mass and notable changes in the growth plate, inclu

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

93 esistance exercise might maintain or improve bone mass and prevent fractures, and that functional str

94 hat deletion of Myc in osteoclasts increases bone mass and protects mice from ovariectomy-induced (OV

95 ication of type I procollagen, without which bone mass and quality are abnormal and fractures and con

96 and bone degeneration may result in reduced bone mass and quality, leading to greater fracture risk.

97 as replaced with phenylalanine had increased bone mass and reduced osteoclast activity.

98 Bone mass and remodeling were evaluated by dual beam X-r

99 ht accelerate age-related loss of muscle and bone mass and resultant sarcopenia and osteopenia.

100 as inadequate bone formation results in low bone mass and skeletal fragility, and over-exuberant ost

101 r the JAKi for 2-4 months resulted in higher bone mass and strength and better bone microarchitecture

102 cytic Panx1 deletion (Panx1(Deltaot)) alters bone mass and strength in female mice.

103 n osteoblasts and osteocytes notably reduced bone mass and strength in mice.

104 (Scl-Ab) treatment leads to improvements in bone mass and strength, as well as enhanced fracture rep

105 e observed significant increases in cortical bone mass and strength, notably in cortical tissue miner

106 x-/-) mice resulted in age-related switch of bone mass and strength.

107 reased, and inhibition leading to decreased, bone mass and strength.

108 f excess glucocorticoids, and the effects on bone mass and structure were evaluated.

109 ation of bone remodeling to maintain healthy bone mass and structure.

110 at the postnatal maintenance of osteoclasts, bone mass and the bone marrow cavity involve iterative f

111 g adolescence is recommended to promote peak bone mass and thereby reduce fracture risk in later life

112 positive effects on bone as shown by higher bone mass and trabecular bone volume, number, and thickn

113 t roles from BMPR1A and ACVR1 in maintaining bone mass and transducing BMP signaling.

114 It acted as an ERalpha agonist on trabecular bone mass and uterine weight, whereas no effect was seen

115 ase mineral apposition rate, bone formation, bone mass, and bone strength, as well as expedite fractu

116 act, female HeyL null mice display increased bone mass, and Hey2 inactivation is developmentally leth

117 proximately 50% reduction in body weight and bone mass, and impaired longitudinal bone growth.

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

119 ated that Cpdm mice additionally display low bone mass, and that this osteopenia is corrected by Tnf

120 latory vs inhibitory actions of estrogens on bone mass are not fully explained by direct effects on b

121 nce throwing activities ceased, the cortical bone mass, area, and thickness benefits of physical acti

122 of IRE1alpha in bone marrow cells increases bone mass as the result of defective osteoclastic bone r

123 radiol increased the trabecular and cortical bone mass as well as the uterine weight, whereas it redu

124 I, Li et al. report that VSG rapidly reduces bone mass, as observed in humans, via rapid demineraliza

125 R-23a cluster gain-of-function mice have low bone mass associated with decreased osteoblast but incre

126 The increase in bone mass associated with RXR deficiency was due to lack

127 of TCDD exposure before achievement of peak bone mass (assumed to occur 2 years after onset of menar

128 risk who have evidence of significantly low bone mass at these sites at the time of KTx.

129 n transgenic C57BL/6J mice resulted in lower bone mass at three ages and greater in vitro osteoclasto

130 Despite comparable baseline indices of bone mass, bone loss caused by hormonal or RANKL perturb

131 ort, we found that Mysm1-/- mice had a lower bone mass both in long bone and calvaria compared with t

132 exhibit the expected reductions in postnatal bone mass but also exhibit an increase in body fat with

133 nitors and osteoclasts functions to optimize bone mass but at distinct bone compartments and in respo

134 O mice diminishes the deficits in trabecular bone mass but not muscle.

135 This is not caused by low bone mass, but by defective bone material.

136 p12(-/-) mice exhibited a slight increase in bone mass, but Dap12(-/-) mice, lacking another ITAM pro

137 groups showed reduced tibia trabecular (Tb) bone mass by 15%, 70%, and 75%, respectively compared to

138 ing, and highlight a potential regulation of bone mass by animal lectins.

139 Loss of Lrp4 in OB-lineage cells increases bone mass by elevating bone formation by OBs and reducin

140 le in bone we analyzed femoral and vertebral bone mass by micro-computed tomography analysis, which s

141 2 activation by disruption of Keap1 improved bone mass by regulating bone remodeling in male mice.

142 ary, PTH administration to CR mice increased bone mass by shifting lineage allocation toward osteogen

143 We confirmed the increased bone mass caused by inhibition of osteoclast activity an

144 lications such as protection against loss of bone mass, chronic diseases, skin cancer, prostate cance

145 male mice had higher trabecular and cortical bone mass compared to age and sex-matched control C57Bl/

146 ) and C5aR2(-/-) mice displayed an increased bone mass compared to wild-type controls due to reduced

147 re smaller in size and have markedly reduced bone mass compared to WT.

148 g over STAT1 downstream of gp130 in this low bone mass condition, and this may have therapeutic value

149 arget gene for therapeutic approaches in low bone mass conditions.

150 Affected patients have a high bone mass coupled with a distinctive appearance where th

151 te GWAS analyses of total body lean mass and bone mass density in children, and show genetic loci wit

152 gated the effects of a 14-day spaceflight on bone mass, density and microarchitecture in weight beari

153 last numbers, and Phlpp1 deficiency enhances bone mass despite higher osteoclast numbers because it a

154 otential new target for the treatment of low bone mass disorders, such as osteoporosis.

155 apeutic approach to reduce the burden of low bone mass disorders.

156 ognized pathophysiological mechanism of high-bone-mass disorders.

157 se mice also develop approximately 50% lower bone mass due to increased osteolysis, but there is no s

158 itamin D supplementation during pregnancy on bone mass during lactation in Brazilian adolescent mothe

159 rotein are essential to achieve optimal peak bone mass during skeletal growth and to prevent bone los

160 Wild type mice lost significant muscle and bone mass during the 33 d spent in microgravity.

161 novel and safe intervention to optimize peak bone mass during youth, alone or in conjunction with oth

162 The powerful regulation of bone mass exerted by the brain suggests the existence of

163 ight, whereas no effect was seen on cortical bone mass, fat mass, or thymus weight.

164 we show herein that FasL-deficient mice lose bone mass following ovariectomy indistinguishably from F

165 h a relatively gracile skeleton (i.e., lower bone mass for our body size).

166 increased in bones, and increased trabecular bone mass from pre-osteoblast specific Ezh2 deletion (Ez

167 Fracture risk is determined by bone mass, geometry, and microstructure, which result fr

168 kd1 and Taz exhibited additive decrements in bone mass, impaired osteoblast-mediated bone formation,

169 We showed significantly increased bone mass in 30-d SPI-fed young rats compared with contr

170 ent; however, the ability of PEDF to restore bone mass in a mouse model of OI type VI has not been de

171 has not yet been proven to improve offspring bone mass in a randomised controlled trial.

172 tion, maintaining homeostasis and a constant bone mass in adult life.

173 with evidence that Sirt1 activators increase bone mass in aged mice, our results also suggest that Si

174 Currently, the cause underlying low bone mass in AIS remains elusive.

175 PTH significantly increased bone mass in all cohorts despite calorie restrictions.

176 hat GH treatment significantly increased Tb. bone mass in all four groups.

177 igate associations between stimulant use and bone mass in children and adolescents.

178 s to examine the effects of stimulant use on bone mass in children.

179 GH treatment increased vertebral Tb. bone mass in Control and UL groups but not in the TBI or

180 ing this function to be associated with high bone mass in humans similar to patients lacking sclerost

181 of ERalpha in the arcuate nucleus increases bone mass in intact and ovariectomized females, confirmi

182 childhood is a significant predictor of peak bone mass in male but not female subjects.

183 iant, nonresorbing osteoclasts and increased bone mass in male mice and protected female mice from bo

184 We report opposing effects of MMnet genes on bone mass in mice and osteoclast multinucleation/resorpt

185 pared the effects of ACVR2B/Fc on muscle and bone mass in mice exposed to Folfiri.

186 as associated with reduced bone strength and bone mass in mice.

187 in an osteoblast-specific manner, increased bone mass in mice.

188 s to arrested osteoclast maturation and high bone mass in mice.

189 follicle-stimulating hormone (Fsh) increases bone mass in mice.

190 ong survival in tumor hosts, and to increase bone mass in models of osteogenesis imperfecta and muscu

191 gh ACVR2A, directly and negatively regulates bone mass in osteoblasts.

192 is by stromal cells in culture and increased bone mass in osteoporotic mice in vivo.

193 cate that the observed age-related switch of bone mass in p47(phox)-deficient mice occurs through an

194 n of the Wnt antagonist sclerostin increases bone mass in patients with osteoporosis and in preclinic

195 e observed a dramatic increase in trabecular bone mass in postnatal mice, which was due to a marked i

196 ssification center and localized increase of bone mass in proximal metaphysis of tibiae.

197 n who were healthy weight for the accrual of bone mass in response to an extra 3 servings dairy/d com

198 Antibiotic significantly improved decreased bone mass in SCD mice mainly through enhanced osteoblast

199 e formation and thus cancellous and cortical bone mass in skeletally mature rodents.

200 Vertebra also showed reduced Tb. bone mass in TBI, UL and TBI-UL groups.

201 atment failed to increase bone formation and bone mass in Tgif1-deficient mice.

202 d high bone formation, which results in high bone mass in the appendicular and axial skeleton.

203 This low bone mass in the mutant mice was secondary to a decrease

204 that OPG expression in chondrocyte increases bone mass in the proximal metaphysis of tibiae through n

205 are co-occurring risk factors for decreased bone mass in the young, particularly in low socioeconomi

206 rs that increase fracture risk include lower bone mass in type 1 diabetes and compromised skeletal qu

207 is uncertain whether vitamin D predicts peak bone mass in young adults.The purpose of this longitudin

208 est that osteocytic Panx1 deletion increases bone mass in young and old female mice and muscle mass i

209 h colonization of adult mice acutely reduces bone mass, in long-term colonized mice, an increase in b

210 We hypothesize that the effects of Pb on bone mass, in part, come from depression of Wnt/beta-cat

211 t support the development and maintenance of bone mass include calcium, vitamin D, protein, potassium

212 The data confirmed the decreased bone mass, increased tartrate-resistant acid phosphatase

213 langeal syndrome frequently present with low bone mass indicating TRPS1 involvement in bone homeostas

214 st haploinsufficiency did not rescue the low bone mass induced by high glucocorticoids.

215 ailty and preventing reduction in muscle and bone mass induced by weight loss.

216 Bone mass is acquired in the pediatric age range, thus i

217 Low bone mass is associated with increased fracture risk, an

218 Adult bone mass is controlled by the bone formation repressor

219 Bone mass is determined by the balance between bone form

220 Bone mass is maintained by the balance between the activ

221 Although IG9402 did not prevent the loss of bone mass, it partially prevented the loss of strength,

222 The low bone mass (LBM) phenotype is the result of both the oste

223 ommon skeletal disorder characterized by low bone mass leading to increased bone fragility and fractu

224 Moreover, T63 markedly protected against bone mass loss in the ovariectomized and dexamethasone t

225 tions, C6-deficient mice displayed a reduced bone mass, mainly because of increased osteoclast activi

226 fibronectin) and low-density lipoprotein-5 (bone mass marker) were down-regulated at M12 in OVX-Diet

227 by high rates of bone resorption and loss of bone mass, may benefit from treatments that inhibit oste

228 (OH)D] at different developmental stages and bone mass measured at age 20 y.Participants were offspri

229 spite knowledge the gut microbiota regulates bone mass, mechanisms governing the normal gut microbiot

230 e and PTPROt knockout mice exhibited similar bone masses, mice in which a putative C-terminal phospho

231 dose of tea polyphenols in achieving better bone mass, microarchitecture integrity, and bone strengt

232 W into a 1-year study to evaluate changes in bone mass, microarchitecture, biomechanical competence,

233 of a Piezo1 agonist to adult mice increased bone mass, mimicking the effects of mechanical loading.

234 Conversely, mice expressing a high bone mass mutant Lrp5 allele are leaner with reduced pla

235 bone structure in women exposed before peak bone mass (n=219), with stronger associations in those e

236 r bone structure in women exposed after peak bone mass (n=48) than in other women (n=18).

237 the administration of alphaKG increases the bone mass of aged mice, attenuates age-related bone loss

238 eta antibody, significantly improved the low bone mass of Esl-1(-/-) mice, suggesting that elevated T

239 Experiment on the ground, the bone mass of humerus, femur and tibia was measured using

240 al vitamin D status has been associated with bone mass of offspring in many, but not all, observation

241 e of maternal deficiencies in the growth and bone mass of offspring is poorly understood.

242 ity in ISS significantly induced the loss of bone mass on humerus and tibia, compared with artificial

243 of MAGP2 alone does not significantly alter bone mass or architecture, and loss of MAGP2 in tandem w

244 onditions, there were minimal differences in bone mass or bone cells between PAR1 KO and WT mice.

245 t of PolgA(mut/mut) mice showed no effect on bone mass or mineralised matrix formation in vitro.

246 ating recent hormonal exposures such as high bone mass or obesity.

247 Nur77 deletion leads to low bone mass owing to augmented osteoclast differentiation

248 Oxt receptor (Oxtr) have opposing effects on bone mass: Oxtr(-/-) mice have osteopenia, and Avpr1alph

249 one formation), significant loss in alveolar bone mass ( P < 0.01), and a sharp reduction in cellular

250 deficiency decreased cortical and trabecular bone mass parameters, suggesting that Hdac3 regulates co

251 s (MKs) in the bone marrow results in a high bone mass phenotype and inhibits skeletal metastasis for

252 Furthermore, the bone mass phenotype in Smurf2- and Smurf1-deficient mice

253 Four weeks-old patDp/+ mice develop a low bone mass phenotype in the appendicular but not the axia

254 This low bone mass phenotype is accompanied by a pronounced incre

255 More notably, this high bone mass phenotype is reversed by the deletion of Oxtr

256 Despite Lpar1(-/-) mice displaying a low bone mass phenotype, we demonstrated that bone marrow ce

257 nia, and Avpr1alpha(-/-) mice display a high bone mass phenotype.

258 in sensitivity despite development of a high bone mass phenotype.

259 These mice developed a severe low-bone-mass phenotype with onset in the second month and i

260 that conditional loss of En1 results in low bone mass, probably as a consequence of high bone turnov

261 the 2.3-kb Col1a1 promoter, showed a gain of bone mass relative to control littermates.

262 In contrast, bone turnover and bone mass remained unchanged in tg arthritic mice.

263 inly by a substantial increase in trabecular bone mass, resulting in improved bone strength of verteb

264 In postmenopausal women with low bone mass, romosozumab was associated with increased bon

265 significantly lower trabecular and cortical bone mass, serum and bone marrow PDGF-BB concentrations,

266 In intact tibiae, ALN increased bone mass significantly more than PTH did.

267 severe osteopenia ( approximately 60% lower bone mass) similar to mice globally expressing the knock

268 d bone turnover, which culminates in reduced bone mass, similar to cases of postmenopausal osteoporos

269 to coordinate with effector cells to adjust bone mass, size, and shape to conform to mechanical dema

270 This large and rapid increase in bone mass suggest that this high dose regimen might prov

271 tolvaptan, does not affect bone formation or bone mass, suggesting that Avpr2, which primarily functi

272 tion resulted in greater gains in total-body bone mass than did placebo.

273 paratide would stimulate larger increases in bone mass than those observed in the DATA study.

274 activity were more important determinants of bone mass than was early-life undernutrition in this pop

275 Pb-exposed animals had decreased bone mass that resulted in bones that were more suscepti

276 , and microstructure, which result from peak bone mass (the amount attained at the end of pubertal gr

277 e osteoblast lineage leads to an increase in bone mass through a dual mechanism: increased osteoblast

278 e novel coupling ECM components that control bone mass through sequestration of TNFalpha and/or RANKL

279 radiol increased the trabecular and cortical bone mass to a similar extent in both Wnt16(-/-) and WT

280 of microbial metabolism, restores IGF-1 and bone mass to levels seen in nonantibiotic-treated mice.

281 educed the total body BMD and the trabecular bone mass to the same degree in Obl-Wnt16 mice and WT mi

282 cise-training period would affect muscle and bone mass together.

283 bers accompanied by a significant decline in bone mass under physiological conditions.

284 ug discovery towards therapeutic targets for bone mass upregulation.

285 The decreased bone mass was neither due to the changes in osteoblastic

286 educed in mice deficient for G-CSF; however, bone mass was not influenced.

287 icro-computed tomography (muCT), and the all bone mass was significantly increased in 2G compared wit

288 inhibition of both factors further increases bone mass, we engineer a first-in-class bispecific antib

289 Differences in bone mass were associated with increased bone formation

290 (21 females aged 10-30 y) with Thal and low bone mass were randomly assigned to receive 25 mg Zn/d o

291 ations were associated with higher childhood bone mass, whereas carbohydrate intake and homocysteine

292 l stress is essential for the maintenance of bone mass, whereas excess mechanical stress induces bone

293 osteoporosis-pseudoglioma syndrome with low bone mass, whereas heterozygous gain-of-function mutatio

294 f RCAN1 or RCAN2 in mice resulted in reduced bone mass, which is associated with strongly increased o

295 on site family (WNT)16 is a key regulator of bone mass with high expression in cortical bone, and Wnt

296 in growth retardation and markedly decreased bone mass with impaired OB differentiation.

297 ose/lipid metabolic derangement, and reduced bone mass with increased bone resorption.

298 letion of Wnt1 in osteocytes resulted in low bone mass with spontaneous fractures similar to that obs

299 AT5 conditional knockout mice showed reduced bone mass, with an increased number of osteoclasts.

300 led to dramatic increases in both muscle and bone mass, with effects being comparable in ground and f