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1 membranous ossification to form skull bones (calvaria).
2 eration by examining critical defects in rat calvaria.
3 Using RT-PCR, we detected DSPP mRNA in mouse calvaria.
4 c mice leads to increased apoptosis in their calvaria.
5 mary murine osteoblastic cells isolated from calvaria.
6 using primary bone cells from newborn mouse calvaria.
7 nd decreased mineralization in newborn mouse calvaria.
8 MSCs (EPC/otMSCs) were fixed to the exposed calvaria.
9 o following RANKL or LPS injections over the calvaria.
10 g, was observed in Gli3(Xt-J/Xt-J) embryonic calvaria.
11 ed that Satb2 was down-regulated in Osx-null calvaria.
12 fibers were found in the diploe of the adult calvaria.
13 ntal defect in bones, most strikingly in the calvaria.
14 surgical control consisted of the intact rat calvaria.
15 ctin/SPARC, biglycan, and type I collagen in calvaria.
16 sed to heal a critical-sized defect in mouse calvaria.
17 , were also increased in miR-433 decoy mouse calvaria.
18 l as primary osteocytes and osteoblasts from calvaria.
19 Osteoblasts were isolated from fetal rat calvaria.
20 stic cell line, UMR-106, as well as in mouse calvaria.
21 -sized defect in the rat (Rattus norvegicus) calvaria.
22 rding the filling of critical defects in rat calvaria.
23 enile (2-day-old) and adult (60-day-old) rat calvaria.
24 he CNC have complete cleft secondary palate, calvaria agenesis, and other skull defects with complete
26 onate inhibition of bone resorption in mouse calvaria also is blocked by mevalonate whereas clodronat
28 mRNA was greater in mutant than in wild-type calvaria and bone marrow, suggesting a compensatory mech
29 ate, but do exhibit developmental defects in calvaria and clavicles that persist through post-natal g
31 er 3 weeks, animals were euthanized, and the calvaria and overlying soft tissues were processed for d
32 acts as a repressor in the developing murine calvaria and that Dlx5, Runx2 type II isoform (Runx2-II)
33 ed greater BrdU incorporation than wild-type calvaria and that Osx overexpression in C2C12 mesenchyma
36 formation when injected locally over murine calvaria, and enhanced trabecular bone formation when ad
37 eoblasts in organ cultures of neonatal mouse calvaria, and in vivo using a mouse model that closely r
41 nusual form of ErbB3 in the context of mouse calvaria as well as osteoblasts in vitro and the femur m
43 last activity, measured using a rat neonatal calvaria assay, increased in the presence of nelfinavir
44 he hypomorphic clavicles and undemineralized calvaria associated with Runx2 haploinsufficiency, where
45 pendent loss of calcium from cultured murine calvaria at porin concentrations in the range of 1 to 10
46 old increase in new woven bone formed in the calvaria at sites of previous bone resorption was observ
47 ry osteocytes isolated from wild-type murine calvaria but not in cells isolated from mice deficient i
51 Furthermore, MIP-1 delta treatment of murine calvaria caused increased bone resorption as determined
52 sponsiveness to PTH was elevated in cultured calvaria cells expressing high levels of osterix, anothe
53 -locked 1alpha,25(OH)2-lumisterol3 analog in calvaria cells were blocked by three cytoplasmic kinase
57 ability to induce bone formation in the rat calvaria critical-size bone defect; therefore, they may
59 Animals were sacrificed after 22 or 44 days, calvaria decalcified and stained with hematoxylin and eo
62 screte morphological features of the Manot 1 calvaria demonstrate that this partial skull is unequivo
64 orphogenic protein 2, the OBs from TIEG(+/+) calvaria displayed several mineralized nodules in cultur
65 rison of HSCs and putative HSC niches in the calvaria, epiphyses, and diaphyses, at steady state or a
68 Ca 2b cells did not induce bone formation in calvaria from mice lacking the Wnt co-receptor Lrp5.
69 minid 1 (KNM-LH 1) is a Homo sapiens partial calvaria from site GvJm-22 at Lukenya Hill, Kenya, assoc
70 nofluorescent staining of bacterium-infected calvaria (i.e., skull bone) demonstrated the presence of
73 rrects the abnormal femoral growth plate and calvaria in organ cultures from embryos of the Fgfr3Y367
74 CaMKII antagonists, using the newborn mouse calvaria in vivo model, cause a 50% decrease in osteobla
75 RANKL were absent in metatarsal explants or calvaria in vivo, respectively, from Mmp9(-/-) mice, dem
80 olysis in vivo were analyzed using the mouse calvaria model, in which AdLacZ was used as the control.
84 age, and tendon, but is barely detectable in calvaria, notochord, or neural retina at select stages o
91 mation when injected subcutaneously over the calvaria of mice and increased cancellous bone volume wh
92 ected into the subcutaneous tissue overlying calvaria of mice lacking IL-1 receptor type I (IL-1RI(-/
94 response following RANKL injection over the calvaria of NLRP12-deficient chimeric mice compared with
95 into the subcutaneous tissues overlying the calvaria of normal mice once daily for 6 days and then e
96 A-III cells were inoculated over the abraded calvaria of nude mice, large tumors formed with invasion
97 miRNAs that are differentially expressed in calvaria of the E18.5 Osx(-/-) embryos compared to wild
99 n and OPG ligand mRNA levels were altered in calvaria of transgenic mice in a pattern that would prom
101 rate that attenuation of Fgfr signaling in a calvaria organ culture with an Fgfr inhibitor prevents p
102 inhibits terminal mineralization in primary calvaria osteoblast cultures when added at early stages
105 culturing mouse bone marrow cells with mouse calvaria osteoblasts, we found by molecular cloning and
112 independent biological assay involving mouse calvaria (skull bone) primary cell cultures, in which a
114 Our data supported a model that within the calvaria sutures Twist1 homodimers (T/T) reside in the o
116 erived from regions of the fetal mandible or calvaria that do not undergo endochondral ossification f
118 cell isolation protocol employed human fetal calvaria tissue sequentially digested with trypsin and c
119 re, we show that p45-sErbB3 stimulated mouse calvaria to secrete factors that increased the invasiven
120 larly, intramembranous bone formation on the calvaria was reduced 60% in COX-2(-/-) mice following in
122 ression in mouse phalangeal chondrocytes and calvaria, which suggests a role of TBC1D24 in skeletogen
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