ライフサイエンスコーパス: bone mass

1 T16 surprisingly increases mainly trabecular bone mass.

2 e associations between dietary acid load and bone mass.

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

4 teocyte viability to strength independent of bone mass.

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

6 rder characterized by bone fragility and low bone mass.

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

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

9 exhibit elevated bone resorption and reduced bone mass.

10 f osteoclastogenesis, resulting in increased bone mass.

11 and suggests potential therapies to increase bone mass.

12 ssue characterized by bone fragility and low bone mass.

13 eoclastic bone resorption to maintain normal bone mass.

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

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

16 ice exhibit lower bone resorption and higher bone mass.

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

18 al inactivity are both associated with lower bone mass.

19 ncreased risk of osteosarcoma, and decreased bone mass.

20 eoclastogenic deficit and reduces trabecular bone mass.

21 etary intake during pregnancy with childhood bone mass.

22 tes did not influence cancellous or cortical bone mass.

23 ed the hypothesis that Pb negatively affects bone mass.

24 calcium intake may adversely affect maternal bone mass.

25 ntrations were not associated with childhood bone mass.

26 for osteoporosis and other conditions of low bone mass.

27 sma zinc, which has been associated with low bone mass.

28 should maximize the potential for growth and bone mass.

29 ing its risk associated with diseases of low bone mass.

30 stration increases systemic and craniofacial bone mass.

31 ased lysosomal gene expression and increased bone mass.

32 exhibit an approximately 5-fold increase in bone mass.

33 correlated with the age-related decrease in bone mass.

34 n of function lead to a striking decrease in bone mass.

35 ew that stimulate bone formation and restore bone mass.

36 exhibited bone fragility, suggesting loss of bone mass.

37 bone mineral density and reduced trabecular bone mass.

38 l pathways are involved in the regulation of bone mass.

39 recognized window of opportunity to optimize bone mass.

40 of activin receptor signaling in regulating bone mass.

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

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

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

44 e a potential therapeutic target to increase bone mass.

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

46 nervous system activation leads to decreased bone mass.

47 ded markedly reduced trabecular and cortical bone mass.

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

49 cally in postnatal mice increased trabecular bone mass.

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

51 cted children and adolescents did not affect bone mass accrual despite significant increases in serum

52 of vitamin D and calcium supplementation on bone mass accrual in HIV-infected youth.

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

54 Bone mass accrual is a major determinant of skeletal mas

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

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

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

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

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

60 body weight, body length, organ weight, and bone mass acquisition were all decreased, reflecting the

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

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

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

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 mice, we show here a significant decrease in bone mass and alterations in cancellous bone structure.

68 alendronate and monthly ibandronate, improve bone mass and are comparable in safety for osteoporosis

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

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

71 The disruption Pb has on bone mass and bone homeostasis is principally explained

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

73 thyroid hormone (PTH) dramatically increases bone mass and currently is one of the most effective tre

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

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

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

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

78 rly postnatal life increases the risk of low bone mass and fracture later in life.

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

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

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

82 nflammatory diseases are associated with low bone mass and fractures during childhood, and may hasten

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

84 osis-like phenotype characterized by reduced bone mass and increased bone marrow fat.

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

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

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

88 Once-weekly alendronate improves bone mass and is well tolerated in these patients, but t

89 one resorption, resulting in suboptimal peak bone mass and mechanical properties associated with low

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

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

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

93 (120 mg/kg once a day for 28 days) improved bone mass and microarchitecture in the lumbar spine and

94 to serum, leading to better preservation of bone mass and mineralization.

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

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

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

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

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

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

101 gnaling in osteocytes that exhibit increased bone mass and remodeling, recognized skeletal effects of

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

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

104 Low bone mass and strength lead to fragility fractures, for

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

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

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

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

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

110 CD248(-/-) mouse tibiae had higher bone mass and superior mechanical properties (increased

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 Reduced bone mineral density, lower femoral bone mass, and altered trabecular bone architecture were

116 n protein (DC-TBPro) derived from BIA water, bone mass, and body volume.

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

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

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

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

121 itor pyridostigmine increases ACh levels and bone mass apparently by inhibiting bone resorption.

122 sms underlying effects of muscle activity on bone mass are largely unknown.

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

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

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

126 autophagy with age may contribute to the low bone mass associated with aging.

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

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

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

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

135 st, Notch activation in osteocytes increases bone mass, but the mechanisms involved and exact functio

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

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

138 F508del mutation in CFTR impacts trabecular bone mass by reducing bone formation.

139 We measured childhood total body bone mass by using dual-energy X-ray absorptiometry at t

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

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

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

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

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

145 /-)) or AMPKalpha2 (Prkaa2(-/-)) had reduced bone mass compared with the WT mice, although the reduct

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

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

148 Bone mass declines with age but the mechanisms responsib

149 in adult mice, whereas epiphyseal cancellous bone mass decreased with loading in both young and adult

150 dose of 1 (mg/kg)/day body weight increased bone mass density and volume, expression of osteogenic g

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

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

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

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

157 ver, potential effects of CLA and calcium on bone mass during a period of bone loss have not been rep

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

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

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

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

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

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

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

167 al for autophagy, from osteocytes caused low bone mass in 6-month-old male and female mice.

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

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

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

171 arly adulthood and is the key determinant of bone mass in adulthood.

172 growth factor in the bone matrix, maintains bone mass in adulthood.

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

174 rption resulted in a profound enhancement of bone mass in Avpr1alpha(-/-) mice and in wild-type mice

175 -Ale increased trabecular bone formation and bone mass in both xenotransplantation studies and in imm

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

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

178 ic reduction of both trabecular and cortical bone mass in homozygous mutants.

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

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

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

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

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

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

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

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

187 We propose that the increased bone mass in nestin-ERalpha(-/-) mice is mediated via de

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

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

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

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

192 ermine the effect of zinc supplementation on bone mass in patients with Thal.

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

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

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

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

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

198 The increased bone mass in the Foxo-deficient mice was accounted for b

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

200 lead to an increase in the prevalence of low bone mass in the offspring later in life.

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

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

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

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

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

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

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

208 Metaphyseal bone mass increased with loading in young mice, but not

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

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

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

212 Peak bone mass is achieved in adolescence/early adulthood and

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

214 It has generally been assumed that bone mass is controlled by endocrine mechanisms and the

215 Adult bone mass is controlled by the bone formation repressor

216 Bone mass is controlled through a delicate balance betwe

217 Bone mass is determined by the balance between bone form

218 Bone mass is maintained by the balance between the activ

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

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

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

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

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

224 tors significantly associated with childhood bone mass, maternal phosphorus intake and homocysteine c

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

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

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

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

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

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

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

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

233 in Ahr(-/-) cells, consistent with the high bone mass noted in Ahr(-/-) male mice.

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

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

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

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

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

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

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

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

242 ferentiation culminated in a high trabecular bone mass pathology.

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

244 The high bone mass phenotype in nestin-ERalpha(-/-) mice was main

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

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

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

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

249 d bone resorption and recapitulated the high bone mass phenotype of Ahr(-/-) mice.

250 own of Shn3 in adult mice resulted in a high-bone mass phenotype, providing evidence that transient b

251 s-pseudoglioma syndrome) or positively (high-bone mass phenotype, sclerosteosis and Van Buchem diseas

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

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

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

255 loss of function leads to a reciprocal high-bone-mass phenotype.

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

257 nd resorption, whereas AMPKalpha2 KO-induced bone mass reduction was largely attributable to elevated

258 stablish a primary role for Avp signaling in bone mass regulation, but also call for further studies

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

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

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

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

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

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

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

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

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

268 ietary factors are associated with childhood bone mass, suggesting that fetal nutritional exposures m

269 recent diagnosis of HIV infection have lower bone mass than controls.

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

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

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

273 hibited increased osteoblast number and high bone mass that was maintained in old age as well as decr

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

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

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

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

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

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

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

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

282 The low bone mass was correlated with significantly decreased os

283 The lumbar spine bone mass was measured in 45 consecutive patients (24 ma

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

285 d pronounced osteopenia in control mice, but bone mass was preserved in mice harboring the Notch acti

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

287 osteoporosis and osteomyelitis cause loss of bone mass, we focused on comparing the dynamics of these

288 Differences in bone mass were associated with increased bone formation

289 (21 females aged 10-30 y) with Thal and low bone mass were randomly assigned to receive 25 mg Zn/d o

290 acid (CLA) has been shown to improve overall bone mass when calcium is included as a co-supplement.

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 We evaluated the association of bone mass with human immunodeficiency virus (HIV) infect

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

298 ment with loss of mammary fat pads, and high bone mass with loss of bone marrow fat, indicating the c

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

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