ライフサイエンスコーパス: bone turnover

1 stic regression after adjustment for age and bone turnover.

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

3 e adolescent runners with normal or abnormal bone turnover.

4 tinuation results in bone loss and increased bone turnover.

5 was determined periodically using markers of bone turnover.

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

7 b caused sustained suppression of markers of bone turnover.

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

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

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

11 ith changes in bone metabolism and increased bone turnover.

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

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

14 tion in pathologic conditions of accelerated bone turnover.

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

16 reduced bone resorption evidenced by reduced bone turnover.

17 CON continued to have or developed decreased bone turnover.

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

19 abnormalities of increased and disorganized bone turnover.

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

21 e mineral density and biochemical markers of bone turnover.

22 r resorbing OCs in regions undergoing active bone turnover.

23 econdary outcomes were changes in markers of bone turnover.

24 17beta-estradiol also resulted in increased bone turnover.

25 ion but did not alter other markers of serum bone turnover.

26 F-L may play an important role in modulating bone turnover.

27 easures were body composition and markers of bone turnover.

28 s associated with a considerable increase in bone turnover.

29 rptiometry (DXA); and biochemical markers of bone turnover.

30 rednisolone reduces synovitis and suppresses bone turnover.

31 itropic hormones, and biochemical markers of bone turnover.

32 ey atrophy, hyperphosphatemia, and increased bone turnover.

33 tion markers was consistent with accelerated bone turnover.

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

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

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

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

38 Sex hormones are linked to inflammation and bone turnover.

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

40 g transitions as were biochemical markers of bone turnover.

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

42 significant effect on bone density but slows bone turnover.

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

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

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

46 ient animals show decreased serum markers of bone turnover.

47 ransplant recipients is associated with high bone-turnover.

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

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

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

51 There was less bone turnover among women with hand OA and/or knee OA.

52 nopause results in a substantial increase in bone turnover and a critical imbalance between bone form

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

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

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

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

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

58 Bone turnover and bone quality were assessed with bioche

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

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

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

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

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

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

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

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

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

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

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

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

71 vestigated by immunohistochemistry to assess bone turnover and metabolism.

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

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

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

75 >1.4/incompressible) was associated with low bone turnover and pronounced osteoblast resistance to pa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 e density of the hip, biochemical markers of bone turnover, and the incidence of new vertebral fractu

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

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

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

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

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

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

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

98 Bone turnover assessed by microcomputer tomography revea

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

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

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

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

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

104 Their bone turnover biomarker pattern is consistent with an in

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

106 The bone turnover biomarkers N-terminal telopeptide and oste

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

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

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

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

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

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

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

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

115 rmone (PTH) regulates mineral metabolism and bone turnover by activating specific receptors located o

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

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

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

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

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

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

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

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

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

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

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

127 Bone turnover comprises two processes: the removal of ol

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

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

130 Markers of bone turnover decreased significantly in the alendronate

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

154 only 100%, suggesting an early uncoupling of bone turnover in favor of formation.

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

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

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

158 The now well-documented acceleration of bone turnover in osteoarthrosis decreases the stiffness

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

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

161 t of soy protein with isoflavones on bone or bone turnover in perimenopausal women.

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

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

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

165 Bone turnover in vivo is regulated by mechanical forces

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 Denosumab reduces bone turnover markers and increases bone mineral density

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

189 Bone turnover markers are not used for diagnosis of oste

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

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

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

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

194 Bone turnover markers can be measured on several occasio

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

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

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

198 Bone turnover markers decreased with denosumab treatment

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

200 Bone turnover markers followed a similar pattern, and no

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

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

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

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

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

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

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

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

209 s were not associated with concentrations of bone turnover markers or changes in BMD in lactating wom

210 Reduction in bone turnover markers was greater with denosumab.

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

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

213 emoral BMD, PTHrP, prolactin, estradiol, and bone turnover markers were measured at 2 wk and at 2, 4,

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

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

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

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

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

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

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

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

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

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

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

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

226 Outcomes included bone mineral density and bone turnover markers.

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

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

229 Altered bone turnover may be a diagnostic or therapeutic target

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

231 netics in determining calcium absorption and bone turnover may become an important research area.

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

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

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

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

236 The reduction in the markers of bone turnover (OC) and synovial tissue turnover (HA and

237 replacement and then assessing the impact on bone turnover of withdrawing both T and E, withdrawing o

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

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

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

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

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

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

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

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

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

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

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

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

250 creases in bone mineral status, increases in bone turnover rate, and reductions in urinary calcium ex

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

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

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

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

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

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

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

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

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

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

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

280 Bone turnover was reduced with risedronate.

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

282 Serum markers of bone turnover were also determined.

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

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

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

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

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

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

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

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

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

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

293 ion of osteoclasts explains the reduction in bone turnover, whereas decreased production and apoptosi

294 that are consistent with an acceleration of bone turnover, which appears to be a part of the pathoph

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

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

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

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.