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1 .R3S), in a male patient with coronal suture synostosis.
2 n EFNA4 are a cause of non-syndromic coronal synostosis.
3 ry formation and the pathogenesis of coronal synostosis.
4 ee of 81 patients with non-syndromic coronal synostosis.
5 performed in 26 patients with single-suture synostosis.
6 n young infants with sagittal and unicoronal synostosis.
7 hould be tested for in patients with coronal synostosis.
8 meeting end-on-end, possibly contributing to synostosis.
9 syndrome, typically associated with coronal synostosis.
10 ions in Tcf12 and Twist1 have severe coronal synostosis.
11 inantly occurred in individuals with coronal synostosis and accounted for 32% and 10% of subjects wit
12 enerated a mouse model of frontonasal suture synostosis and midfacial hypoplasia through the tissue-s
13 e performed in six patients with multisuture synostosis, and 61 studies were performed in 26 patients
15 r patients with TWIST mutations, are coronal synostosis, brachycephaly, low frontal hairline, facial
16 of normal exhibit postnatal multiple-suture synostosis; by contrast, embryonic calvarial development
17 n and extensive posterior cervical vertebral synostosis, cardiac septal defects with valve dysplasia,
18 ory subluxation, congenital occipitocervical synostosis, congenital unilateral absence of C1, odontoi
19 ed clinical disorder include multiple-suture synostosis, craniofacial dysmorphism, Chiari malformatio
20 transgenic newborn mice (with mild sagittal synostosis) demonstrated continuous bone growth and over
21 karyocytic thrombocytopenia with radio-ulnar synostosis, familial platelet syndrome with predispositi
26 als from 20 unrelated families where coronal synostosis is due to an amino acid substitution (Pro250A
28 mature fusion of these bones, termed coronal synostosis, is a common human developmental anomaly.
29 onatal growth retardation and death, coronal synostosis, ocular proptosis, precocious sternal fusion,
31 bilateral humeral hypoplasia, humeroscapular synostosis, pelvic abnormalities, and proximal defects o
35 cal functioning of individuals with sagittal synostosis (SS) are highly disparate, limiting their cli
37 ant disorders of joint development, multiple synostosis syndrome (SYNS1) and a milder disorder proxim
38 ta establish locus heterogeneity in multiple-synostosis syndrome and demonstrate that the disorder ca
41 r, in a cohort of six probands with multiple-synostosis syndrome, only one was found to be heterozygo
42 ctyly C, the protein encoded by the multiple-synostosis-syndrome allele was secreted as a mature GDF5
43 us Tcf12; Twist1 mice display severe coronal synostosis, the individual role of Tcf12 had remained un
45 urrence of proximal symphalangism and carpal synostosis, we identified six different point mutations
46 main clinical manifestations include coronal synostosis, widely spaced eyes, clefting of the nasal ti
47 ional reconstructive techniques for sagittal synostosis with the long-term vision of optimizing the m