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1 ore often in the interparietal bone than the parietal bone.
2  in two midsagittal calvarial defects in the parietal bone.
3 anial remains, particularly in occipital and parietal bones.
4  reduced frontal bones, just anterior to the parietal bones.
5 hymal cells participate in the growth of the parietal bones.
6 ith a tongue of neural crest between the two parietal bones.
7 st-derived frontal bone and mesoderm-derived parietal bone accompanies coronal suture fusion during e
8 sm, resulting in relative enlargement of the parietal bones and anterior displacement of the cerebell
9 e were assessed in ex vivo cultures of mouse parietal bones and in an in vivo model in which TLR2 ago
10 ation and differentiation in the frontal and parietal bones and in the coronal suture.
11 nd amniotic fluid and electrodes beneath the parietal bones and in the nuchal muscle were used to mon
12 e marrow in the ribs, cervical vertebra, and parietal bone are 0.81, 0.80, and 0.55 for 6-MeV alpha-p
13 females still had decreased bone mass in the parietal bone at 90 days.
14 niosynostosis, the fusion of the frontal and parietal bones at the coronal suture.
15 ietal foramina (PFM) are oval defects of the parietal bones caused by deficient ossification around t
16 lls adjacent to the osteogenic fronts of the parietal bones could differentiate towards the osteoblas
17 defect in chick cranial skeleton, especially parietal bone development in the presence of high glucos
18 -induced increases in ALP and osteocalcin in parietal bone extracts of IGF-I KO mice were comparable
19  images revealed a lytic lesion in the right parietal bone, filled with an oval-shaped, large, extra-
20 ol of this promoter is sufficient to enhance parietal bone growth into the sagittal suture by P6.
21 velopment, including the rate of frontal and parietal bone growth, and the boundary between sutural a
22 ontal bones are neural crest-derived and the parietal bones mesodermal, with a tongue of neural crest
23 on of IGFBP-5 to the outer periosteum of the parietal bone of IGF-I KO mice increased ALP activity an
24                              At 90 days, the parietal bone of transgenic males was of normal width, s
25 ular defects were created in the frontal and parietal bones of NOD/SCID mice and treated with Ink-Bon
26                    We also reconstructed the parietal bones of OH 7 and estimated its endocranial vol
27  accompanied by expansion of the frontal and parietal bones of the skull vault and deployment of the
28 rtical bone porosity, marked thinning of the parietal bones of the skull, and a high incidence of fra
29 ineral release and matrix degradation in the parietal bone organ cultures by increasing differentiati
30 and Pam3 stimulated RANKL in osteoblasts and parietal bone resorption.
31 d mesodermal origin, forming the frontal and parietal bones, respectively.
32  RvE1 treatment of uniform craniotomy in the parietal bone significantly accelerated regeneration of
33 in are found to occur more frequently in the parietal bone than the interparietal bone, whereas bone
34                  PFM are oval defects of the parietal bones that are also a characteristic feature of
35 did not observe a reduction in the growth of parietal bone to the same degree.
36                                              Parietal bone trabecular compartment was mildly altered.
37 sor cells that contribute to the frontal and parietal bones, we show that Twist1 and EphA4 are requir
38 mation was reduced in cortical bone, and the parietal bones were 45% thinner than in wild-type animal
39  opposing sides of the wild-type frontal and parietal bones, which prefigures later bone overlap at t