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1                                              OPG concentration was measured in the supernatants of T8
2                                              OPG is a decoy receptor for RANKL, thereby increasing BM
3                                              OPG is known to be a high-affinity heparan sulfate (HS)-
4                                              OPG levels were measured in serum or in plasma.
5                                              OPG mRNA expression and protein production do not genera
6                                              OPG mRNA was also significantly increased in biopsy spec
7                                              OPG preference was greater for fixed partial denture pla
8                                              OPGs and orbitofacial neurofibromas are clinically diver
9                                              OPGs may enlarge in later childhood and beyond such that
10                              Serum IL-1beta, OPG, and BALP levels revealed no significant difference
11 588; radiographs and OFS had kappaw = 0.542 (OPG kappaw = 0.555 and I-O kappaw = 0.521).
12 imal models suggest that IL-1b, TNF-a, IL-6, OPG and RANKL may mediate periodontitis in diabetes.
13                        The effects of TSG-6, OPG, and the inflammation mediators TNFalpha, interleuki
14 The expression of wild type GATA-3 activated OPG mRNA and protein expression, while the expression of
15   Although the total amounts of GCF albumin, OPG, IL-17A, and IL-17A/F were similar in the study grou
16 ldren 10 years or younger with NF1 and/or an OPG.
17                             Children with an OPG (sporadic or secondary to neurofibromatosis type 1)
18  -8, RANK, and RANKL and increased BMP-2 and OPG levels in the periodontal tissue.
19 cantly promoted RANKL expression in ABCs and OPG in DPCs.
20 evelopment causing strabismic amblyopia, and OPG) were difficult to treat adequately and tended to ca
21             High levels of serum calcium and OPG are significantly associated with the progression of
22 se and preference of utilisation of CBCT and OPG by various dental practitioners in their clinical pr
23 -sectional study was carried out on CBCT and OPG data of 620 different cases treated by different den
24 olved in apoptosis, such as BBC3, NEDD9, and OPG.
25  at 40 and 104 degrees C), the heated OP and OPG oils showed the highest oxidative stability.
26               The association between PP and OPG remained significant after adjusting for multiple po
27  compared to other dental practitioners, and OPG was advocated for FPD planning, whereas CBCT was adv
28                                    RANKL and OPG concentrations were increased in the OF group at 3 m
29 present in root dentin with robust RANKL and OPG expression.
30 fy a range of cytokines, including RANKL and OPG in sera from 10 patients with diabetes, 12 patients
31 combination, and the expression of RANKL and OPG was measured.
32 mma reduced the production of both RANKL and OPG, and IL-17 had only a modest effect on the expressio
33 ive RT-PCR showed up-regulation of RANKL and OPG, with a 128% increase in RANKL/OPG ratio in bgn(-/0)
34 and samplings, serum and GCF TOS, RANKL, and OPG levels were determined by a novel automatic colorime
35 cTRAILR2 in primary neurons and of TRAIL and OPG in OPCs.
36 een recombinant human (rhTRAIL) variants and OPG.
37 A and colocalization of reactivities to anti-OPG and anti-gp100 (HMB45) antibodies in LAM lung nodule
38 th MDD had significant decreases in baseline OPG/RANKL ratio and in plasma OPN levels.
39 marker genes, including Runx2, ALP, OC, BSP, OPG, and DMP-1, with concurrent upregulation of RANKL, t
40  marrow fibrosis were virtually abolished by OPG treatment, whereas alendronate and zoledronate only
41 uclear factor-kappaB, a process abrogated by OPG.
42 becular osteoclasts was greatly decreased by OPG but not by either alendronate or zoledronate.
43 ural deafness, and renal (HDR) syndrome - by OPG therapy.
44 At the multivariate analysis, serum calcium, OPG, and estimated glomerular filtration rate were the o
45                                  Circulating OPG levels are also important biomarkers of various clin
46 t into the genetic regulation of circulating OPG levels.
47 gerin (OPG)-immunoglobulin fragment complex (OPG-Fc) completely restore the function of fast-twitch e
48                 Using a HS binding-deficient OPG mutant, we further show that in an osteoblast/bone m
49  significantly induced mRNAs for TRAIL, DR5, OPG, and mDcTRAILR2 in primary neurons and of TRAIL and
50                The expression of TRAIL, DR5, OPG, and mDcTRAILR2 was significantly increased after HI
51 de polymorphisms (SNPs) in the gene encoding OPG (TNFRSF11B) are associated with traveler's diarrhea
52 0 kb upstream of the TNFRSF11B gene encoding OPG and another new locus on chromosome 17q11.2 were sig
53      During the course of injury, endogenous OPG appears to suppress the effects of RANKL.
54  stimulated by ATRA was blocked by exogenous OPG, and mRNA expression of genes associated with bone f
55 prevented by the co-treatment with exogenous OPG.
56 -) mice with recombinant osteoprotegerin (Fc-OPG) or vehicle for 5 months.
57                            Treatment with Fc-OPG significantly reduced the calcified lesion area with
58  of Cryptosporidium infection and a role for OPG in modulating this host response.
59                          OEBFs prepared from OPG-knock-out mice exhibited a similar effect, indicatin
60 g children with and without vision loss from OPGs.
61 al detachment) or the afferent system (e.g., OPG), and 12 patients had correctable refractive errors.
62                   Furthermore, serum and GCF OPG concentrations were lower in the periodontitis group
63 01; P <0.0001; P = 0.032, respectively), GCF OPG (P = 0.036), and serum and saliva sRANKL (P <0.0001)
64  A SNP in the exon 1 region of the OPG gene (OPG+1181G>C) was associated with TD in white travelers w
65                   Using an Nf1 optic glioma (OPG) GEM model, we report novel defects in non-selective
66 , aged 4-28 years) had optic pathway glioma (OPG) in addition to OFNF.
67                       Optic pathway gliomas (OPGs) and orbitofacial plexiform neurofibromas are two o
68  50% of children with optic pathway gliomas (OPGs) experience visual impairment, and few regain their
69 g young children with optic pathway gliomas (OPGs) for visual deterioration can be difficult owing to
70         Children with optic pathway gliomas (OPGs) frequently experience vision loss from their tumor
71     The management of optic pathway gliomas (OPGs) remains controversial.
72 s type 1 (NF1) and/or optic pathway gliomas (OPGs).
73 in the optic pathway (optic pathway gliomas, OPGs), especially in children with the neurofibromatosis
74  a pre-specified objective performance goal (OPG).
75             In the etidronate-treated group, OPG expression was significantly expressed and osteoclas
76                    T84 cells produced higher OPG levels in response to infection with various diarrhe
77 g analysis revealed that upon binding of HS, OPG undergoes a dramatic conformational change, resultin
78 resent here three lines of evidence that HS, OPG, and RANKL form a stable ternary complex.
79          However, the molecular detail of HS-OPG interaction remains poorly understood, which hinders
80                     Importantly, we identify OPG as a HIF target gene capable of directing osteoblast
81                              Most important, OPG-Fc combined with a low dose of formoterol, a member
82        However, despite marked improvements, OPG-Fc was not as effective in preventing the loss of fu
83 whereas the increase in mTEC availability in OPG-deficient (Tnfrsf11b(-/-)) mice impacts the intrathy
84                                 Mutations in OPG are involved in a variety of human diseases.
85              No differences were observed in OPG expression among groups.
86                AT1R silencing also increased OPG gene expression in HGF only.
87 -4 suppressed RANKL expression and increased OPG expression, IFNgamma reduced the production of both
88    ATV reduced RANKL and DKK-1 and increased OPG, WNT10b, and beta-catenin expressions and BALP activ
89 licated in human trials; moreover, increased OPG levels have been consistently associated with the in
90  mice exhibited a similar effect, indicating OPG-independent inhibition.
91 ients significantly suppressed Wnt3a-induced OPG expression and enhanced RANKL expression in osteobla
92      In addition, we show that Wnt3a-induced OPG expression was diminished in osteoblasts cocultured
93 expression of TFAP2B and the RANK inhibitor, OPG, in human breast cancer correlate and are associated
94 rable receptor activator of NF-kappaB ligand/OPG ratio, in addition to known anti-inflammatory and pr
95                         Moreover, by mapping OPG expression to a subset of Aire(+) mTEC, our data sho
96 rgic cell projections to the striatum in Nf1 OPG mice in vivo.
97   The reduction in striatal DA levels in Nf1 OPG mice is associated with reduced striatal expression
98                            Specifically, Nf1 OPG mice exhibit reduced rearing in response to novel ob
99               We demonstrate that female Nf1-OPG mice exhibit greater retinal ganglion cell (RGC) los
100                      In addition, female Nf1-OPG mice have threefold more microglia than their male c
101 ects the retinal abnormalities in female Nf1-OPG mice.
102  outcome, we leveraged Nf1 optic glioma (Nf1-OPG) mice.
103 , as ovariectomy, but not castration, of Nf1-OPG mice normalizes RGC survival and RNFL thickness.
104                         Neither pegTNFRI nor OPG could significantly halt the osteophytic responses i
105 ith PGE2 stimulation, reduced RANKL, but not OPG, expression.
106 saccharide is able to induce dimerization of OPG monomers with a stoichiometry of 1:1.
107                   The differential effect of OPG versus bisphosphonates on marrow fibrosis, despite s
108 n of CTX and induced increased expression of OPG in unstressed animals with PD.
109 also produced OPG, as shown by expression of OPG mRNA and colocalization of reactivities to anti-OPG
110 resumably, HS could regulate the function of OPG and affect how it inhibits RANKL.
111 imated that over half of the heritability of OPG levels could be explained by all variants examined i
112 rophage co-culture system, immobilization of OPG by HS at the osteoblast cell surface substantially l
113 ecretion without affecting PTH inhibition of OPG expression, and it does so by blocking HDAC4 proteas
114 c muscles but is rescued by the injection of OPG-Fc.
115 cells secrete OPG at high levels and lack of OPG causes sensorineural hearing loss in addition to the
116 pothesized that these cellular mechanisms of OPG may be involved in the growth and proliferation of l
117 tiple myeloma cell lines, in the presence of OPG secreted by stromal cells.
118 ls, there was an early peak in production of OPG mRNA protein.
119 ng increase for RANKL and TRAP; reduction of OPG and leukocytosis, which were significantly prevented
120          In order to study the regulation of OPG expression, we conducted a database search on regula
121 w of Col2a1-Opg mice, suggesting the role of OPG in blocking the differentiation of early mesenchymal
122                       The protective role of OPG, in animal models, against vascular calcification ha
123 re seems to be some dichotomy in the role of OPG, RANKL, and tumor necrosis factor-related apoptosis-
124  we report mapping of the HS-binding site of OPG.
125 rtments and that represent direct targets of OPG-mediated control.
126 tantially lowers the inhibitory threshold of OPG toward RANKL.
127 ebral arteriopathy risk with the presence of OPGs.
128          Recent advances in the treatment of OPGs include chemotherapeutic, radiation-based, and surg
129 sphatidylethanolamine and glucose added oil (OPG).
130 slational levels, and it showed no effect on OPG expression in calvarial osteoblasts.
131 jection of anti-RANKL antibody (P < 0.05) or OPG-Fc (P < 0.01), but not L6-Fc, into rat gingival papi
132 on of optic nerve disease due to glaucoma or OPG and to the possibility that vision might be improved
133  modest effect on the expression of RANKL or OPG.
134               Young children with NF1 and/or OPGs were frequently unable to complete recognition acui
135  clinical trial for children with NF1 and/or OPGs.
136                             Osteoprotegerin (OPG) is a glycoprotein that acts as a decoy receptor for
137                             Osteoprotegerin (OPG) is a key regulator of bone remodeling.
138                             Osteoprotegerin (OPG) is a marker and regulator of arterial calcification
139                             Osteoprotegerin (OPG) is involved in bone homeostasis and tumor cell surv
140                             Osteoprotegerin (OPG), a decoy receptor secreted by osteoblasts, is a maj
141                             Osteoprotegerin (OPG), a soluble receptor of the cytokine TNF-related apo
142                             Osteoprotegerin (OPG), an immunoregulatory member of the TNF receptor sup
143     Interleukin (IL)-1beta, osteoprotegerin (OPG), and bone-specific alkaline phosphatase (BALP) seru
144 -kappa B ligand (RANKL); 2) osteoprotegerin (OPG); 3) interleukin (IL)-6; and 4) tumor necrosis facto
145 ibroblast growth factor 23, osteoprotegerin (OPG), fetuin A, and clinical and biochemical parameters.
146 line phosphatase (ALP), and osteoprotegerin (OPG) by hMSCs and transcriptome analysis demonstrated up
147  kappa B ligand (RANKL) and osteoprotegerin (OPG) immunohistochemistry was carried out, and the RANKL
148  necrosis factor-alpha, and osteoprotegerin (OPG) in HGF and HPLF.
149 -17E, IL-17F, IL-17A/F, and osteoprotegerin (OPG) in women with rheumatoid arthritis (RA), osteoporos
150 r-kappaB ligand (RANKL) and osteoprotegerin (OPG) levels and RANKL/OPG ratios in serum and gingival c
151 F-kappaB ligand (RANKL) and osteoprotegerin (OPG) production by ST2 cells, despite MLO-Y4 cells suppo
152 F-kappaB ligand (RANKL) and osteoprotegerin (OPG) signaling in osteocytes was not studied in sheep.
153 ), RANK ligand (RANKL), and osteoprotegerin (OPG) signaling pathway (RANKL/RANK/OPG signaling) is imp
154 -kappaB ligand (RANKL), and osteoprotegerin (OPG) that modulate bone homeostasis.
155 ), RANK ligand (RANKL), and osteoprotegerin (OPG) were also investigated by immunohistochemistry to a
156 -kappaB ligand (RANKL), and osteoprotegerin (OPG) were analyzed in the furcation area of mandibular m
157 r-kappaB ligand (RANKL) and osteoprotegerin (OPG) were assessed by enzyme-linked immunosorbent assay
158  Kappa B Ligand (RANKL) and osteoprotegerin (OPG), positive and negative regulators of osteoclast dif
159 eptor type I (pegTNFRI) and osteoprotegerin (OPG), respectively, affected bony spur formation.
160 d activity are regulated by osteoprotegerin (OPG), bisphosphonates suppress osteoclast activity but n
161 pression but >2-fold higher osteoprotegerin (OPG) expression than donor-matched ABCs, yielding a RANK
162 ntly higher RANKL and lower osteoprotegerin (OPG) mRNA and increased RANKL:OPG ratio.
163 effects on bone metabolism, osteoprotegerin (OPG), a soluble member of the tumor necrosis factor fami
164 on of interleukin-6 but not osteoprotegerin (OPG), an inhibitor of RANKL.
165  ES increased expression of osteoprotegerin (OPG) and the OPG/RANKL ratio.
166 ivity of TSG-6 with that of osteoprotegerin (OPG) and to investigate its role as an autocrine modulat
167  suppress the expression of osteoprotegerin (OPG) in osteoblasts and subsequently potentiate osteocla
168 ntly enhanced expression of osteoprotegerin (OPG) without inducing change in receptor activator of NF
169             Serum levels of osteoprotegerin (OPG), a decoy receptor for RANKL, steadily increased ove
170 ed that daily injections of osteoprotegerin (OPG)-immunoglobulin fragment complex (OPG-Fc) completely
171 and and decreased levels of osteoprotegerin (OPG).
172 gh the direct regulation of osteoprotegerin (OPG).
173 kappa-B ligand (RANKL)-RANK-osteoprotegerin (OPG) signaling associated with bone resorption.
174 RANK), RANK-ligand (RANKL), osteoprotegerin (OPG), and osteocalcin was performed.
175 ctor kappaB ligand (RANKL), osteoprotegerin (OPG), and tartrate-resistant acid phosphatase (TRAP) wer
176 tor-kappa B ligand (RANKL), osteoprotegerin (OPG), and tartrate-resistant acid phosphatase (TRAP).
177 ctor-kappaB ligand (RANKL), osteoprotegerin (OPG), tartrate-resistant acid phosphatase (TRAP), and ac
178 ctor-kappaB ligand (RANKL), osteoprotegerin (OPG), wingless (WNT) 10b, dickkopf-related protein 1 (DK
179 or kappaBeta ligand (RANKL)/osteoprotegerin (OPG) (2.5 +/- 0.7-fold, p < 0.001) ratio.
180  (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) axis and expression of the transcriptional regulato
181 of NF-kappaB ligand (RANKL)/osteoprotegerin (OPG), tumor necrosis factor alpha (TNF-alpha), and IL-1b
182 d the TRAIL decoy receptors osteoprotegerin (OPG), mDcTRAILR1, and mDcTRAILR2 were determined.
183 ression and down-regulating osteoprotegerin (OPG) production.
184 ative ratios of sclerostin, osteoprotegerin (OPG), and receptor activator of nuclear factor-kappaB li
185 tor-kappaB ligand (sRANKL), osteoprotegerin (OPG), a proliferation-inducing ligand (APRIL), B-cell ac
186 or-kappa B ligand (sRANKL), osteoprotegerin (OPG), B-cell activating factor (BAFF), and a proliferati
187 luble RANK ligand (sRANKL), osteoprotegerin (OPG), cathepsin-K, and sclerostin.
188 rs of bone inflammation-the osteoprotegerin (OPG)-RANK-RANKL system or osteopontin (OPN)-play a role
189 nd bone metabolism markers (osteoprotegerin [OPG], osteocalcin, procollagen type I N-terminal propept
190 stic increase in the preference of CBCT over OPG in recent times.
191               We report 4 cases of pediatric OPGs (2 neurofibromatosis type 1-related and 2 sporadic
192 a showed that among the dental practitioners OPG was more commonly ordered by general dentists (31%)
193 study showed that general dentists preferred OPG and CBCT compared to other dental practitioners, and
194               LAM lung nodules also produced OPG, as shown by expression of OPG mRNA and colocalizati
195 the in vivo function of chondrocyte-produced OPG in osteoclast formation and postnatal bone growth ha
196 KL antibody, osteoprotegerin fusion protein (OPG-Fc), or a control fusion protein (L6-Fc) into gingiv
197 he investigation, 143 panoramic radiographs (OPGs) and 77 intra-oral radiographs (I-Os) were evaluate
198                In addition to the RANKL-RANK-OPG signaling axis, other factors produced by osteoblast
199 cell fusion and activation by the RANKL/RANK/OPG and ATP-P2RX7-IL1 pathways; and (3) regulatory mecha
200 data provide direct evidence that RANKL/RANK/OPG signaling is modulated in patients with CN and plays
201 otegerin (OPG) signaling pathway (RANKL/RANK/OPG signaling) is implicated in the osteolysis associate
202 ecules - including IL-1, IL-6, IL-17, RANKL, OPG, and CCL2 - modulate probiotic action.
203                    Systemic levels of RANKL, OPG, and inflammatory cytokines (interleukin-8, granuloc
204  likely to have regulation of the RANK-RANKL-OPG axis as their goal.
205 ting the osteoclast activation via the RANKL-OPG axis, without interfering with bone anabolism.
206 ulating osteoclastogenesis through the RANKL-OPG pathway, or indirectly by downregulating canonical W
207 y in osteoblasts, at least through the RANKL-OPG pathway.
208 on than donor-matched ABCs, yielding a RANKL/OPG ratio of 41:1 (ABCs:DPCs).
209  increased the expression of RANKL and RANKL/OPG ratio by mesenchymal stem cells at 2 h.
210 nomous increase in SOST/sclerostin and RANKL/OPG ratio in the setting of unloading.
211 ) and osteoprotegerin (OPG) levels and RANKL/OPG ratios in serum and gingival crevicular fluid (GCF)
212 nt results reveal that TOS, RANKL, and RANKL/OPG values are systemically and locally increased in per
213          Serum and GCF TOS, RANKL, and RANKL/OPG values were higher in the periodontitis groups compa
214 nd it helps in restoring the decreased RANKL/OPG ratio in adult mice.
215 blished that chondrocytes also express RANKL/OPG and support osteoclast formation.
216 ast differentiation through expressing RANKL/OPG cytokines.
217                             The global RANKL/OPG ratio in the spine after 8 months of steroid and die
218       All test groups presented higher RANKL/OPG(+) cells than the control group around ligated/unlig
219 RANKL and OPG, with a 128% increase in RANKL/OPG ratio in bgn(-/0)fmod(-/-) TMJs.
220 deficient osteoclasts had an increased RANKL/OPG ratio, providing a positive feedback loop that incre
221  that C3(-/-) BM cells exhibited lower RANKL/OPG expression ratios, produced smaller amounts of macro
222 study aimed to investigate the role of RANKL/OPG in MAC in patients with CN.
223 nd activity by increasing the ratio of RANKL/OPG in osteoblasts.
224                   We mainly focused on RANKL/OPG signalling, the TNF and TNF receptor superfamilies a
225                          The perturbed RANKL/OPG ratio in RRV-infected OBs may therefore contribute t
226  arising due to imbalances in the RANK/RANKL/OPG molecular pathway, and due to the progressive weaken
227          The infection alters the RANK/RANKL/OPG signalling dynamics that regulates osteoblasts and o
228 , assessment of the osteocyte-specific RANKL/OPG ratio showed that the steroid-induced osteoporosis i
229                     Differences in the RANKL/OPG Axis in vivo, and RANKL-induced maturation of osteoc
230 in level may be more reliable than the RANKL/OPG ratio as a diagnostic and prognostic marker of perio
231 eep model of osteoporosis to study the RANKL/OPG ratio correlation to the method of osteoporosis indu
232 dontal disease in rats, decreasing the RANKL/OPG ratio in gingival connective tissue and reducing alv
233 teal bone resorption by increasing the RANKL/OPG ratio via RARalpha receptors, a response that can be
234                                    The RANKL/OPG ratio was also disrupted in mice infected with RRV;
235 istochemistry was carried out, and the RANKL/OPG ratio was calculated.
236                                    The RANKL/OPG ratio was disrupted in the synovial fluid of RRV pat
237                       In addition, the RANKL/OPG ratio was increased by ATRA, release of (45)Ca stimu
238                                    The RANKL/OPG ratio was significantly lower in healthy individuals
239  density of inflammatory cells and the RANKL/OPG ratio were significantly lower (P </=0.05) than in P
240 teoprotegerin (OPG) mRNA and increased RANKL:OPG ratio.
241 bly because of marked reduction in the RANKL:OPG ratio in the MN1 null cells.
242                                    The RANKL:OPG ratios are shifted in favor of bone protection by IL
243 f GATA-3 or a GATA-3 shRNA construct reduced OPG mRNA and protein levels.
244 cal Wnt signaling, disrupted Wnt3a-regulated OPG and RANKL expression in osteoblasts.
245 t that HS plays an active role in regulating OPG-RANKL interaction and osteoclastogenesis.
246 modeling by direct actions on bone, rescuing OPG production and restoring a favorable receptor activa
247                                  Sclerostin, OPG, and RANKL levels were measured by enzyme-linked imm
248                               The sclerostin/OPG and sclerostin/RANKL ratios were significantly lower
249  that cochlear spiral ganglion cells secrete OPG at high levels and lack of OPG causes sensorineural
250                                        Serum OPG concentrations were significantly higher in the simv
251                                        Serum OPG was significantly higher in LAM patients than in nor
252 nally analyzed the association between serum OPG and PP in a prevalent cohort of 969 KTX patients (me
253 vastatin is associated with increasing serum OPG concentrations, and this could have a protective eff
254 ) scores, and GCF APRIL, serum sRANKL, serum OPG, and sRANKL concentrations in TM groups (P <0.05).
255                       We conclude that serum OPG is independently associated with pulse pressure in k
256        Furthermore, IL-3 increases the serum OPG level in adult mice.
257      PP was positively correlated with serum OPG (rho = 0.284, p < 0.001).
258                                      sRANKL, OPG, and IL-17 levels were determined by enzyme-linked i
259 iva, and serum levels of IL-6, IL-8, sRANKL, OPG, BAFF, and APRIL were determined by enzyme-linked im
260  results are suggestive of a role of sRANKL, OPG, and sclerostin as prognostic biomarkers in peri-imp
261 differences in GCF concentrations of sRANKL, OPG, IL-17A, IL-17E, IL-17F, and IL-17A/F.
262              Concentrations of RANK, sRANKL, OPG, and sclerostin were significantly increased in pati
263                         Serum sRANKL, sRANKL/OPG, and IL-17A/IL-17E ratios were significantly higher,
264                                   The sRANKL/OPG ratios were significantly higher in the RA group tha
265                                     Stronger OPG immunolabeling and weaker RANKL immunolabeling were
266 vantages of CBCT over 2D imaging techniques (OPG).
267         Based on these data, it appears that OPG may have tumor-promoting roles in the pathogenesis o
268                Our results demonstrated that OPG expression in chondrocyte increases bone mass in the
269           Here we tested the hypothesis that OPG is associated with increased pulse pressure.
270 ne and cardiac tissues, we hypothesized that OPG-Fc, a bone and skeletal muscle protector, acts syner
271                         Herein, we show that OPG stimulated proliferation of cells cultured from expl
272                      Our study suggests that OPG is secreted by intestinal epithelial cells in respon
273                                          The OPG-RANK-RANKL system plays the principal role in determ
274                                          The OPG/RANKL/receptor activator of nuclear factor kappaB ax
275  expression of osteoprotegerin (OPG) and the OPG/RANKL ratio.
276    Ketamine significantly increased both the OPG/RANKL ratio and plasma OPN levels, and significantly
277 th TSC2 loss of heterozygosity expressed the OPG receptors, receptor activator of NF-kappaB ligand, s
278   Genotyping was performed for 4 SNPs in the OPG gene for 968 North American travelers with or withou
279 teropathogens and that a polymorphism in the OPG gene is associated with an increased susceptibility
280            A SNP in the exon 1 region of the OPG gene (OPG+1181G>C) was associated with TD in white t
281 atory elements in the promoter region of the OPG gene, and identified two potential GATA-3 binding si
282 insight into the complex interactions of the OPG/RANKL/receptor activator of nuclear factor kappaB ax
283                         We conclude that the OPG-RANK-RANKL system and the OPN system play important
284 nfidence bound: 29.9%) versus 43.0% with the OPG (p < 0.0001).
285 splays a significantly decreased affinity to OPG.
286 high effectiveness and diminished binding to OPG.
287                            We therefore used OPG and bisphosphonates to evaluate the extent to which
288 ice after treatment of animals with vehicle, OPG, alendronate, or zoledronate.
289 7E ratios were significantly higher, whereas OPG concentrations were significantly lower in the RA gr
290 5) only for non-smokers at 6 months, whereas OPG was not significant (P >0.05).
291                      We investigated whether OPG is produced by intestinal epithelial cells and teste
292 n in HMOBs in a dose-dependent manner, while OPG protein remained similar to baseline.
293 e 17q11.2 were significantly associated with OPG variation.
294                            Coincubation with OPG, the decoy receptor for RANKL, attenuated osteogenic
295 ements in cortical bone mineral density with OPG in PPR*Tg mice were associated with greater improvem
296                        RANKL inhibition with OPG had little or no effect on osteoblastic differentiat
297                Given that most patients with OPG-related visual impairment will show modest or no vis
298                  TSG-6 acted in synergy with OPG to inhibit RANKL-mediated bone resorption and was pr
299 bevacizumab-based treatment in children with OPGs.
300 er layer thickness inversely correlates with OPGs and decreased vision.

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