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1  equinovarus (CTEV) is the commonest form of clubfoot.
2  of lower extremity abnormalities, including clubfoot.
3 ng PITX1 in a patient with isolated familial clubfoot.
4 at PITX1 haploinsufficiency could also cause clubfoot.
5  that accounts for similar findings in human clubfoot.
6 d in 3 of 66 probands with familial isolated clubfoot.
7 at the locus in a sibling pair with isolated clubfoot.
8 tory" as having a first-degree relative with clubfoot.
9 neural tube defect (0.82, 0.53 to 1.27), and clubfoot (1.06, 0.88 to 1.28).
10 ctively, were hydrocephalus (100% and 100%), clubfoot (100% and 99.8%), injuries or wounds (54.7% and
11                                              Clubfoot, a common major structural malformation, develo
12 h severe infantile epileptic encephalopathy, clubfoot, absent deep tendon reflexes, extrapyramidal sy
13                                              Clubfoot affects 1 in 1000 live births, although little
14 risk factors among 346 infants with isolated clubfoot and 3,029 infants without defects from the Atla
15  of this syndrome combine brain atrophy with clubfoot and arthrogryposis.
16 ilial factors and smoking in the etiology of clubfoot and identifies a potentially important interact
17 relatively common cause of familial isolated clubfoot and provides strong evidence linking clubfoot e
18 table cause of congenital contractures (e.g. clubfoot) and results from mutations in genes that encod
19 ct/patent foramen ovale, neural tube defect, clubfoot, and oral cleft, defined based on validated alg
20 hildren, and babies with a family history of clubfoot, but studies of risks associated with maternal
21 he use of antiviral drugs was more common in clubfoot cases than in controls (odds ratio = 4.22, 95%
22 jor structural malformations (i.e., isolated clubfoot); controls were mothers of 2,037 children born
23 ease, inflammatory arthritis, infection, and clubfoot deformities.
24 ways for future investigations of idiopathic clubfoot etiology in humans.
25 lubfoot and provides strong evidence linking clubfoot etiology to abnormal early limb development.
26 iption factor PITX1 previously implicated in clubfoot etiology.
27  mutations were identified that segregate in clubfoot families.
28 tion, the possibility of this interaction in clubfoot has not been examined.
29 plication segregated with autosomal-dominant clubfoot in all three families but with reduced penetran
30 wo congenital malformations were identified: clubfoot in one twin, and cardiac malformation in a sing
31                                              Clubfoot is a common musculoskeletal birth defect for wh
32                                              Clubfoot is one of the most common severe musculoskeleta
33             The genetic etiology of isolated clubfoot (iTEV) remains unclear.
34                                     No overt clubfoot-like deformity was observed in Prrx1-cre;Fstl5L
35   Peroneal artery hypoplasia occurred in the clubfoot limb and corresponded spatially with small late
36  deletion segregated with autosomal dominant clubfoot over three generations.
37 a gene involved in early limb development in clubfoot pathogenesis also suggests additional pathways
38 tudy the role of PITX1 haploinsufficiency in clubfoot pathogenesis, we began to breed Pitx1 knockout
39 ers that undermine the outcomes of a Ponseti clubfoot program are primarily poverty and noncompliance
40 symmetric right-sided predominant idiopathic clubfoot segregating as an autosomal-dominant condition
41 ht-sided involvement in tibial hemimelia and clubfoot suggests that PITX1, or pathways involving PITX
42                         Talipes equinovarus (clubfoot, TEV) is a congenital rotational foot deformity
43 quaint the reader with the Ponseti method of clubfoot treatment and to describe the features of the t
44 ique that make it superior to other forms of clubfoot treatment.
45                         Ponseti treatment of clubfoot was available at 46% (95% 38.8-53.2) of distric
46  mice were previously reported to be normal, clubfoot was observed in 20 of 225 Pitx1(+/-) mice, resu
47                                              Clubfoot was unilateral in 16 of the 20 affected Pitx1(+
48 padias, hydrocephalus, cleft lip/palate, and clubfoot) was determined by physical examination.
49  identify the genes responsible for isolated clubfoot, we screened for genomic copy-number variants w
50 ale, population-based, case-control study of clubfoot with detailed information on maternal medicatio
51      Cases were 646 mothers of children with clubfoot without other major structural malformations (i