ライフサイエンスコーパス: bone turnover

1 w microenvironment, imposed by the stages of bone turnover.

2 t S. aureus triggers profound alterations in bone turnover.

3 cancer cells, independently of its effect on bone turnover.

4 emerged as important positive regulators of bone turnover.

5 hose patients with low (n=18) or high (n=17) bone turnover.

6 ient animals show decreased serum markers of bone turnover.

7 stic regression after adjustment for age and bone turnover.

8 ing lt 1300 mg Ca than did those with normal bone turnover.

9 for serum 25-hydroxyvitamin D and markers of bone turnover.

10 e adolescent runners with normal or abnormal bone turnover.

11 tinuation results in bone loss and increased bone turnover.

12 was determined periodically using markers of bone turnover.

13 ts were not observed in mature mice with low bone turnover.

14 erved with APOE alleles on BMD or markers of bone turnover.

15 b caused sustained suppression of markers of bone turnover.

16 d hormone axis (THA), muscle metabolism, and bone turnover.

17 ls and have decreased pain in states of high bone turnover.

18 t play key roles in regulating bone mass and bone turnover.

19 ith changes in bone metabolism and increased bone turnover.

20 ecific G(s)alpha deficiency leads to reduced bone turnover.

21 d properties of bone, skeletal geometry, and bone turnover.

22 y training may have chronic implications for bone turnover.

23 bsorption, and disease-related imbalances in bone turnover.

24 reduced bone resorption evidenced by reduced bone turnover.

25 CON continued to have or developed decreased bone turnover.

26 the spine and hip and biochemical markers of bone turnover.

27 abnormalities of increased and disorganized bone turnover.

28 n has been shown in early studies to inhibit bone turnover.

29 e mineral density and biochemical markers of bone turnover.

30 ey atrophy, hyperphosphatemia, and increased bone turnover.

31 r resorbing OCs in regions undergoing active bone turnover.

32 econdary outcomes were changes in markers of bone turnover.

33 17beta-estradiol also resulted in increased bone turnover.

34 tion in pathologic conditions of accelerated bone turnover.

35 control both physiological and pathological bone turnover.

36 tion markers was consistent with accelerated bone turnover.

37 ), prostate-specific antigen, and markers of bone turnover.

38 complex effects of T-cell reconstitution on bone turnover.

39 a like-1 (DLK1) as an endocrine regulator of bone turnover.

40 bone mass, probably as a consequence of high bone turnover.

41 Sex hormones are linked to inflammation and bone turnover.

42 MD), risk of osteoporosis, and biomarkers of bone turnover.

43 g transitions as were biochemical markers of bone turnover.

44 ral density at other sites and in markers of bone turnover.

45 fferential effects depending on the level of bone turnover.

46 significant effect on bone density but slows bone turnover.

47 uring osteoblast-mediated bone formation and bone-turnover.

48 ransplant recipients is associated with high bone-turnover.

49 Bone turnover (activation frequency) was low in 45.6%, n

50 The risk of inducing low bone turnover (adynamic bone) seems to be quite low with

51 se characterised by focal areas of increased bone turnover, affecting one or several bones throughout

52 oth groups of patients experienced decreased bone turnover after KTx, but zoledronate itself did not

53 Therefore, FGF21 is a critical rheostat for bone turnover and a key integrator of bone and energy me

54 In young mice with high bone turnover and an abundance of perivascular osteoprog

55 e health, and adequate intakes may influence bone turnover and balance.

56 s in parathyroid hormone result in increased bone turnover and bone loss.

57 In contrast, bone turnover and bone mass remained unchanged in tg art

58 Growth hormone therapy increased markers of bone turnover and bone mineral density in children with

59 neral retention, the genetic determinants of bone turnover and calcium flux and the impact of the gut

60 in experimental arthritis by inhibiting both bone turnover and cartilage degradation and reducing the

61 mphocytes are essential stabilizers of basal bone turnover and critical regulators of peak bone mass

62 and dentin matrix protein 1, remarkably high bone turnover and defective osteocyte maturation that is

63 explore the influence on this association of bone turnover and genetic factors related to lead toxico

64 is an important enzyme for the modulation of bone turnover and gingival recession.

65 e of the cellular and cytokine mechanisms of bone turnover and glucocorticoid mechanisms of action ar

66 mutations predispose to elevated subchondral bone turnover and hypertrophy in calcified cartilage, ye

67 ion of intravenous zoledronic acid decreases bone turnover and improves bone density at 12 months in

68 t patients leads to excessive suppression of bone turnover and increased incidence of adynamic bone d

69 However, reduced bone turnover and infection, an almost universal finding

70 This rat model characterizes the pattern of bone turnover and inflammation after extraction and bone

71 and, (18)F-NaF PET/CT can indicate increased bone turnover and is generally used in the assessment of

72 gy restriction and whether hormones regulate bone turnover and mass.

73 vestigated by immunohistochemistry to assess bone turnover and metabolism.

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

75 information sensitive for subtle changes in bone turnover and perfusion, which assists the clinical

76 of action, significantly reduce the rate of bone turnover and potentially reduce the efficacy of the

77 monstrate that TCC-mediated effects regulate bone turnover and promote an adequate response to fractu

78 >1.4/incompressible) was associated with low bone turnover and pronounced osteoblast resistance to pa

79 patients with ESRD, PAD associates with low bone turnover and pronounced osteoblast resistance to PT

80 ociated with elevated circulating markers of bone turnover and reduced bone density in women.

81 umab may be similar to IV BPs in suppressing bone turnover and reducing SRE risk.

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

83 se results suggest a possible common role of bone turnover and repair in the early manifestations of

84 dy, we investigated the effect of the TCC on bone turnover and repair.

85 ed marrow microenvironment, which deregulate bone turnover and result in bone loss and skeletal-relat

86 to proceed with additional explorations into bone turnover and skeletal remodeling.

87 or anabolic, and review pathways that affect bone turnover and steps in those pathways that are targe

88 Remaining markers of bone turnover and whole-body bone mineral density and co

89 is associated with vitamin D deficiency, low bone turnover, and abnormalities in calcium homoeostasis

90 ium absorption, kinetically derived rates of bone turnover, and biochemical markers of bone turnover

91 n true fractional calcium absorption (TFCA), bone turnover, and bone-regulating hormones in overweigh

92 data suggest that c-Kit negatively regulates bone turnover, and disrupted c-Kit signaling couples inc

93 resent study shows that low bone volume, low bone turnover, and generalized or focal osteomalacia are

94 nate therapy is highly effective at reducing bone turnover, and it has been shown to heal radiologica

95 ll molecule, leads to a dramatic increase in bone turnover, and they suggest a novel approach to the

96 as beneficial for spine and hip BMD, reduced bone turnover, and was well tolerated.

97 The duration of the suppression of bone turnover appeared to be dose-dependent.

98 to determine whether calcium homeostasis and bone turnover are affected by high-protein diets during

99 er, PTH, and cyclosporine on bone volume and bone turnover are apparently overridden by the prominent

100 renal transplant recipients correlates with bone turnover as it does in postmenapausal osteoporosis.

101 The high protein acid load affected bone turnover, as indicated by higher Ca(2+) and deoxypy

102 Bone turnover assessed by microcomputer tomography revea

103 ride PET with that of biochemical markers of bone turnover assessed over 6 mo.

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

105 ercent change at any BMD site and markers of bone turnover at 12 months.

106 and patients were classified as having high bone-turnover based on elevated urinary levels of at lea

107 ine, there were no differences in markers of bone turnover between the groups.

108 Their bone turnover biomarker pattern is consistent with an in

109 c BMD loss at the lumbar spine (osteocalcin, bone-turnover biomarker, p = 0.0002) and femoral neck (o

110 The bone turnover biomarkers N-terminal telopeptide and oste

111 RCE had no significant effect on other bone turnover biomarkers.

112 significantly higher mean +/- SE markers of bone turnover (bone alkaline phosphatase: 15.8 +/- 0.59

113 ffect of dexlansoprazole and esomeprazole on bone turnover, bone mineral density (BMD), true fraction

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

115 ; expand the osteoblastic pool; and increase bone turnover, bone mineral density, and trabecular bone

116 oporotic phenotype is not due to accelerated bone turnover--both the number and activity of osteoclas

117 PTH levels, provoking a dramatic increase in bone turnover but no net change in bone mineral density.

118 and endothelial cells (ECs) is essential for bone turnover, but the molecular mechanisms of such comm

119 high concentrations of cytokines involved in bone turnover, but vitamin K supplementation did not con

120 PTH modulates bone turnover by binding to the PTH/PTH-related peptide

121 s disease because osteoprotegerin suppresses bone turnover by functioning as a decoy receptor for ost

122 nd width and for markers of inflammation and bone turnover by microcomputed tomography, histology, an

123 ectly correlated with the systemic marker of bone turnover C-telopeptide of type 1 collagen (r=0.6; P

124 n bone mineral status, although increases in bone turnover, calcium absorption, and urinary calcium e

125 Serum markers related to bone turnover, calcium, phosphorus, bone alkaline phosph

126 Diseases that affect the regulation of bone turnover can lead to skeletal fragility and increas

127 nce questions the simplified etiology of low bone turnover causing MRONJ and offers evidence on the p

128 ast pathways, IL-7 is central to the altered bone turnover characteristic of estrogen deficiency.

129 g alendronate had increased serum markers of bone turnover compared with continuing alendronate: 55.6

130 loss in body weight, thymus involution, and bone turnover) compared with standard GCs.

131 Bone turnover comprises two processes: the removal of ol

132 ects, we hypothesized that elevated rates of bone-turnover contribute to posttransplant bone loss in

133 e prevalence of histologically diagnosed low bone turnover decreased from 85.0% to 41.8% in the 1.25

134 s further worsened bone structure, increased bone turnover, depressed osteoblastogenesis (Runx2, Spar

135 not show any qualitative abnormalities, with bone turnover (double labeling) seen in all specimens.

136 Increased subchondral trabecular bone turnover due to imbalanced bone-resorbing and bone-

137 -like growth factor I (IGF-I) and markers of bone turnover during 6 mo of exercise training.

138 by the lactating mammary gland and regulate bone turnover during lactation.

139 reveal a potential role for TMJ subchondral bone turnover during the initial early stages of TMJ OA

140 riol on bone loss and biochemical markers of bone turnover during the second year.

141 Runners with an elevated bone turnover (EBT) (n = 13) had a lower body mass, fewe

142 centrations suggest secondary causes of high bone turnover (eg, bone metastases or multiple myeloma).

143 of the efficacy shown in an in vivo model of bone turnover following once-daily oral administration,

144 alternative method to biochemical markers of bone turnover for investigating the dynamic state of the

145 atients (69%) were classified as having high bone-turnover (Group 1), and 19 patients (31%) were clas

146 esent, they were classified as having normal bone-turnover (group 2).

147 ients (31%) were classified as having normal bone-turnover (Group 2).

148 dy were compared between the high and normal bone-turnover groups.

149 (18)F-NaF, a PET radiotracer of bone turnover, has shown potential as an imaging biomark

150 ctures potentially resulting from suppressed bone turnover have been described as "atypical," affecti

151 of bone turnover, and biochemical markers of bone turnover have increased our knowledge of the pathop

152 ate the resolution phase of inflammation and bone turnover have not been unveiled.

153 the effects of TNF inhibitors on markers of bone turnover; however, few have measured bone mineral d

154 pact treatment and address the importance of bone turnover in cartilage integrity.

155 ts extend earlier findings by accounting for bone turnover in confirming the association between elev

156 gmented DKK1 levels are associated with high bone turnover in diverse low bone mass states in rodent

157 tamin K status was associated with decreased bone turnover in healthy girls consuming a typical US di

158 e osteopenic, suggesting that E may regulate bone turnover in men, as well as in women.

159 (Dose-Response of Gonadal Steroids and Bone Turnover in Men; NCT00114114).

160 Moderate energy restriction increases bone turnover in obese postmenopausal women and may be r

161 s slowed the progression of CAC and improved bone turnover in patients on HD with baseline intact par

162 acebo on BMD and biochemical measurements of bone turnover in patients with PBC-associated bone loss.

163 e C activation is not required for increased bone turnover in response to PTH.

164 mages may be useful for assessing changes in bone turnover in response to therapy.

165 g-term glucocorticoid (GC) administration on bone turnover in two frequently used mouse strains; C57B

166 Bone turnover in vivo is regulated by mechanical forces

167 we found significant increases in markers of bone turnover in women given PPI therapy compared with w

168 his study we evaluated their use to quantify bone turnover in women receiving antiresorptive therapy

169 bone using pre-clinical mouse models of high bone turnover, including estrogen deficiency and sustain

170 Vitamin K modulates cytokines involved in bone turnover, including interleukin-6 (IL-6) and osteop

171 ater axial and peripheral bone mass and less bone turnover, independent of key confounding factors.

172 es have suggested that increased subchondral bone turnover is a determinant of progression of osteoar

173 Abnormal bone turnover is common in CKD, but its effects on bone

174 Oversuppression of bone turnover is probably the primary mechanism for the

175 which regulates mineral ion homeostasis and bone turnover, is a G protein-coupled receptor harboring

176 one regeneration, in contrast to homeostatic bone turnover, is not reliant upon active SIRT3, and our

177 d properties of bone, skeletal geometry, and bone turnover-is high, although heritability of fracture

178 oviral therapy itself has complex effects on bone turnover, it is now evident that the majority of HI

179 Elevated levels of PTH increase bone turnover, leading to either anabolic or catabolic e

180 ased 1,25(OH)(2)D levels not only stimulated bone turnover, leading to osteopenia, but also suppresse

181 Vitamin D supplements decrease PTH and bone turnover marker concentrations among blacks.

182 In untreated women, very high bone turnover marker concentrations suggest secondary ca

183 n of serum calcium levels and suppressed the bone turnover marker serum pyridinoline at day 4 and lat

184 ry end point was percentage of change in the bone turnover marker urine N-telopeptide corrected for u

185 as been shown to have a beneficial effect on bone turnover markers (BTM) in postmenopausal women.

186 bone mineral density (BMD) loss according to bone turnover markers (BTMs) and urinary metabolites.

187 Bone turnover markers (BTMs) demonstrated presence of bo

188 se association between dairy food intake and bone turnover markers and a positive association with bo

189 Plasma bone turnover markers and bone mineral density (BMD) wer

190 Plasma bone turnover markers and bone mineral density (BMD) wer

191 We compared the long-term effects on bone turnover markers and calciotropic hormones of a mul

192 Denosumab reduces bone turnover markers and increases bone mineral density

193 Levels of bone turnover markers and increases in bone mineral cont

194 Bone turnover markers are not used for diagnosis of oste

195 ell designed, prospective studies, including bone turnover markers as intermediary endpoints.

196 his animal model was confirmed by changes in bone turnover markers as well as bone architecture, as m

197 one density (BMD), calciotropic hormones and bone turnover markers at 12, 18, and 24 months after tra

198 cluded change in TH BMD and changes in serum bone turnover markers at month 12.

199 Bone turnover markers can be measured on several occasio

200 Much remains to be learnt about how bone turnover markers can be used to monitor the effect

201 one mineral density and greater reduction in bone turnover markers compared with alendronate; when wo

202 In both groups, serum concentrations of bone turnover markers decreased during year 1 and remain

203 Bone turnover markers decreased with denosumab treatment

204 en groups occurred in any BMD measures or in bone turnover markers during year 1 or year 2.

205 Bone turnover markers followed a similar pattern, and no

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

207 study characterized VA intake, serum VA, and bone turnover markers in postmenopausal women with and w

208 ondary outcomes included clinical variables, bone turnover markers in serum and oral fluid, systemic

209 e determined the bone phenotype and measured bone turnover markers in the murine DS model Ts65Dn.

210 s-sectional data suggest that measurement of bone turnover markers may increase the diagnostic accura

211 In people with osteoporosis, bone turnover markers might be useful to assess the resp

212 pQCT), parathyroid hormone (PTH) levels, and bone turnover markers obtained at baseline and 3, 6, and

213 crog/d) was not consistently associated with bone turnover markers or BMC.

214 Reduction in bone turnover markers was greater with denosumab.

215 density, osteoblast gene markers, and serum bone turnover markers were also elevated.

216 and strength of the bones, and the levels of bone turnover markers were analyzed.

217 Concentrations of hormones and bone turnover markers were measured in serum.

218 Assays for 3 bone turnover markers were performed by using commercial

219 roidism (parathyroid hormone > 130 ng/L) and bone turnover markers were significantly reduced in grou

220 D, falls, circulating calciotropic hormones, bone turnover markers, and adverse events.

221 vitamin D (1,25[OH]2D), parathyroid hormone, bone turnover markers, and minerals and in bone mineral

222 ry end points included bone mineral density, bone turnover markers, and safety outcomes.

223 so examined B-vitamin biomarkers relative to bone turnover markers, bone alkaline phosphatase, and ur

224 Changes in bone turnover markers, bone mineral density (BMD) by dua

225 id-stimulating hormone (TSH) levels and high bone turnover markers, low bone mineral density, and an

226 rough evaluation of bioavailability, safety, bone turnover markers, muscle strength, and quality of l

227 resolution of bone scans, and reductions in bone turnover markers, pain, and narcotic use.

228 Body weight, bone turnover markers, serum parathyroid hormone (PTH),

229 h protein arrays for 14 pro-inflammatory and bone turnover markers, while qPCR was used for detection

230 hway alone, with a corresponding decrease in bone turnover markers.

231 Outcomes included bone mineral density and bone turnover markers.

232 Bone mineral density was higher and bone-turnover markers were lower in the men who received

233 Altered bone turnover may be a diagnostic or therapeutic target

234 Blood lead and bone turnover may be associated with the risk of amyotro

235 However, as increased bone turnover may predict future bone loss and fractures

236 me in suppression of parathyroid hormone and bone turnover might help explain why nutrient interventi

237 s model was conceived as the first step in a bone turnover modeling platform.

238 Markers of bone turnover, N-telopeptides of type 1 collagen, and bo

239 Serum and urinary markers of bone turnover or adrenal function did not predict the de

240 sium citrate supplementation does not reduce bone turnover or increase BMD in healthy postmenopausal

241 exhibit reductions in bone mineral density, bone turnover, osteoclast activation, and impaired bone

242 cute vaso-occlusive crises (VOCs), increased bone turnover, osteoclast activity (RankL), and osteocla

243 fruit and vegetable intake (single-blind) on bone turnover over 2 y.

244 otal dietary protein (per kg) and markers of bone turnover (P < 0.05).

245 high bone-turnover, vs. 1.36+/-0.66%, normal bone-turnover; P=0.006).

246 high bone-turnover, vs. 0.64+/-0.54%, normal bone-turnover; P=0.02) and the hip (-0.69+/-0.38%, high

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

248 n correlated negatively with bone volume and bone turnover (r = -0.32 to -0.59, P < 0.05 to 0.01), wh

249 n factor responsible for low bone volume and bone turnover (r = 0.54 and r = 0.43, P < 0.01).

250 one was primarily lamellar in structure, the bone turnover rate was less than 5 microns/day, and was

251 Consistent with the observations on BMD, the bone turnover rates in both men and women (as measured b

252 ed obesity rates, greater muscle mass, lower bone turnover rates, and advantageous femur geometry.

253 g potential of osteogenic cells leads to low bone turnover rates, producing hyperphosphatemia and VC,

254 Bone turnover remained suppressed.

255 Normal bone turnover requires tight coupling of bone resorption

256 Cells that regulate bone turnover share a common precursor with inflammatory

257 This phenotype is the consequence of a high bone turnover state, with increased endocortical osteocl

258 Bone turnover statistically significantly decreased with

259 Biochemical markers of bone turnover such as bone-specific alkaline phosphatase

260 treating diseases characterized by excessive bone turnover, such as osteoporosis and prosthetic joint

261 volume at the hip, and levels of markers of bone turnover suggest that the concurrent use of alendro

262 ctions in calcium or increases in markers of bone turnover, suggesting this agent is less likely to h

263 ipients with elevated biochemical markers of bone-turnover, suggesting that these markers may be usef

264 tive correlation between dietary protein and bone turnover suggests that increasing protein intakes m

265 ases from baseline in biochemical markers of bone turnover than did placebo (P < 0.001).

266 one volume and greater increases in cortical bone turnover, than did PTH(1-34).

267 he efficacy shown in three in vivo models of bone turnover, the compound was selected for clinical de

268 l density at the total hip and in markers of bone turnover, the time to changes in bone mineral densi

269 icant within-group differences in markers of bone turnover; there was a nonsignificant increase in CT

270 in bone and are ideally located to influence bone turnover through their syncytial relationship with

271 osteoclast differentiation and may regulate bone turnover under conditions in which adenosine levels

272 AT may act to exacerbate inflammation and/or bone turnover under inflammatory conditions such as RA o

273 ups at the lumbar spine (-1.11+/-0.42%, high bone-turnover, vs. 0.64+/-0.54%, normal bone-turnover; P

274 er; P=0.02) and the hip (-0.69+/-0.38%, high bone-turnover, vs. 1.36+/-0.66%, normal bone-turnover; P

275 re numerically identical in both groups, but bone turnover was greater (C-terminal telopeptide levels

276 Bone turnover was lower, and bone density was higher, in

277 Based on the TMV classification, bone turnover was normal in 48%, high in 26%, and low in

278 collagen realignment, matrix deposition, and bone turnover was noted in later stages.

279 No significant decrease in BMD or rise in bone turnover was observed with weight loss at normal or

280 In addition, bone turnover was reduced and bone loss during lactation

281 Bone turnover was reduced with risedronate.

282 Changes in biochemical markers of bone turnover were also analysed in this substudy, and t

283 Serum markers of bone turnover were also determined.

284 Changes in bone turnover were assessed by measurement of serum and

285 eline in BMD and biochemical measurements of bone turnover were assessed.

286 (44)Ca to (42)Ca) and circulating indexes of bone turnover were determined at day 8 (WM) and day 29 (

287 -energy X-ray absorptiometry, and markers of bone turnover were measured before and after weight loss

288 Markers of bone turnover were measured in fasting blood samples.

289 variables related to calcium metabolism and bone turnover were measured.

290 Biochemical parameters of bone turnover were obtained monthly and, bone mineral de

291 Factors related to bone turnover were significant predictors of blood lead

292 Biochemical parameters of bone turnover were similar in both groups at 6 and 12 mo

293 Biochemical markers of bone-turnover were measured at study entry, and patients

294 exhibit accelerated osteoclasts activity and bone turnover, which culminates in reduced bone mass, si

295 er in children than in adults, likely due to bone turnover, which impairs clinical utility in childre

296 omponent characterized by focal increases in bone turnover, which in some cases is caused by mutation

297 Bone turnover, which is determined by osteoclast-mediate

298 e mineral density and biochemical markers of bone turnover with vertebral fracture reduction.

299 and were characterized by focal increases in bone turnover, with increased bone resorption and format

300 the hip, spine, and total body, and reduced bone turnover, with minimal adverse effects.