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1 rietal bone growth, and the boundary between sutural and osteogenic cells.
2 ly: either accelerating it or initiating net sutural bone resorption for various therapeutic objectiv
3 th 2 affected siblings showing a nuclear and sutural cataract was reported in contrast to previously
4 th autosomal dominant congenital nuclear and sutural cataracts was identified and characterized.
5 ome characterized by late-closing fontanels, sutural cataracts, facial dysmorphisms and skeletal defe
6 2.3, in a family with congenital nuclear and sutural cataracts.
7 1 also results in changes in the identity of sutural cells prior to overt osteogenic differentiation,
8  is expressed in a layer of mesoderm-derived sutural cells that lie along the osteogenic-non-osteogen
9  the mutant neurocranium, we found a midline sutural defect and craniosynostosis with abnormal osteob
10 pe, impaired secondary fiber cell migration, sutural defects and thinning of the posterior capsule wh
11 sults show that lens opacities and posterior sutural defects occur when mutant R116C alphaA-crystalli
12  are sufficient to induce lens opacities and sutural defects.
13                             Cranio-lenticulo-sutural dysplasia (CLSD) is an autosomal recessive syndr
14                             Cranio-lenticulo-sutural dysplasia (CLSD) was recently shown to be caused
15 phenotype of individuals with cranio-lentico-sutural dysplasia (CLSD).
16  skeletal disorders such as cranio-lenticulo-sutural dysplasia and osteogenesis imperfect, caused by
17 uctures that are similar to cranio-lenticulo-sutural dysplasia patient cells with SEC23A mutations, w
18 As SEC23A lesions cause the cranio-lenticulo-sutural dysplasia syndrome, crusher provides the first v
19 382L in human Sec23A causes cranio-lenticulo-sutural dysplasia, and we suggest that this mutation dis
20 ollagen deposition defects, cranio-lenticulo-sutural dysplasia, or chylomicron retention disease, but
21 entified from patients with cranio-lenticulo-sutural dysplasia, we discovered that the SEC23-SEC31 in
22 pansion and displacement as a consequence of sutural growth and it can simulate craniosynostosis.
23 nical stimuli have the potential to modulate sutural growth effectively: either accelerating it or in
24 driven pediatric model that explains cranial sutural growth in the pediatric population.
25                                              Sutural growth is accelerated upon small doses of oscill
26                                        Thus, sutural growth is determined by hereditary and mechanica
27 nial bone development as a function of local sutural growth rates, and we inferred its parameters sta
28  mechanical stimuli can effectively modulate sutural growth.
29 rstanding of how mechanical stimuli modulate sutural growth.
30 ne hypoplasia and persistent widening of the sutural joints.
31 nx2-II, and pSmad1/5/8 expression as well as sutural mesenchymal cell proliferation.
32 ones and conversely, what is the fate of the sutural mesenchymal cells when calvarial bones approxima
33 tical event of CS is the early loss of basal sutural mesenchyme as the osteogenic fronts, expressing
34 p-regulation of osteopontin and Fgfr1 in the sutural mesenchyme, down-regulation of Fgfr2, and inhibi
35  Notch2 and the Notch effector, Hes1, in the sutural mesenchyme.
36 uding premature osteogenic conversion of the sutural mesenchyme.
37                The average elastic moduli of sutural mineralization fronts 30 micro m away were signi
38        The elastic properties of sutures and sutural mineralization fronts are potentially useful for
39 acial sutures and their immediately adjacent sutural mineralization fronts have different capacities
40 maticotemporal (ZTS)-and their corresponding sutural mineralization fronts in 8 young New Zealand Whi
41                     Detailed analysis of the sutural morphology of T. roseae suggests that the abilit
42          Our approach consists of defining a sutural morphospace, assigning functional fields to that
43  by nearly threefold through enhancements in sutural remodeling compared with unmodified E2 administr
44 sile and compressive strains induce anabolic sutural responses beyond natural growth.
45  waveforms induce corresponding waveforms of sutural strain.
46  well-developed squamosal bosses and a short sutural surface with the exoccipital-opisthotic complex,
47 a long anterior platform for the nasofrontal sutural surface, which may indicate the presence of a sm
48 us based on the extension of the nasofrontal sutural surface.