Cleft Palate Research Today is a free monthly online journal that collates and summarizes the latest research about Cleft Palate, including details on causes, surgery, treatment.

Initial cleft severity and maxillary growth in patients with complete unilateral cleft lip and palate.

Chiu YT, Liao YF, Chen PK

Division of Craniofacial Orthodontics, Department of Dentistry and Craniofacial Center, Chang Gung Memorial Hospital, Taipei, Taiwan.

Published 1 August 2011 in Am J Orthod Dentofacial Orthop, 140(2): 189-95.
Full-text of this article is available online (may require subscription).

Articles on Cleft Palate published 27 July 2011:

Association of common variants, not rare mutations, in IRF6 with nonsyndromic clefts in a Honduran population.   Laryngoscope, 121(8): 1756-9.

[Abstract] [Full-text]

Articles on Cleft Palate published 26 July 2011:

From birth to maturity: a group of patients who have completed their protocol management. Part III. Bilateral cleft lip-cleft palate.   Plast Reconstr Surg, 128(2): 475-84.

[Abstract] [Full-text]

Articles on Cleft Palate published 25 July 2011:

Predictors of velopharyngeal insufficiency after Le Fort I maxillary advancement in patients with cleft palate.   J Oral Maxillofac Surg, 69(8): 2226-32.

[Abstract] [Full-text]

Articles on Cleft Palate published 20 July 2011:

Structural basis of p63α SAM domain mutants involved in AEC syndrome.   FEBS J, 278(15): 2680-8.

p63 is a member of the p53 tumour suppressor family that includes p73. The p63 gene encodes a protein comprising an N-terminal transactivation domain, a DNA binding domain and an oligomerization domain, but varies in the organization of the C-terminus as a result of complex alternative splicing. p63α contains a C-terminal sterile α motif (SAM) domain that is thought to function as a protein-protein interaction domain. Several missense and heterozygous frame shift mutations, encoded within ... [Abstract] [Full-text]

Articles on Cleft Palate published 18 July 2011:

Deficiency of the cytoskeletal protein SPECC1L leads to oblique facial clefting.   Am J Hum Genet, 89(1): 44-55.

Genetic mutations responsible for oblique facial clefts (ObFC), a unique class of facial malformations, are largely unknown. We show that loss-of-function mutations in SPECC1L are pathogenic for this human developmental disorder and that SPECC1L is a critical organizer of vertebrate facial morphogenesis. During murine embryogenesis, Specc1l is expressed in cell populations of the developing facial primordial, which proliferate and fuse to form the face. In zebrafish, knockdown of a SPECC1L ... [Abstract] [Full-text]

Single-nucleotide polymorphisms (SNPs) of the IRF6 and TFAP2A in non-syndromic cleft lip with or without cleft palate (NSCLP) in a northern Chinese population.   Biochem Biophys Res Commun, 410(4): 732-6.

Non-syndromic cleft lip with or without cleft palate (NSCLP) is a common birth defect that is presumably caused by genetic factors alone or gene alterations in combination with environmental changes. A number of studies have shown an association between NSCLP and single-nucleotide polymorphisms (SNPs) in the interferon regulatory factor 6 (IRF6) gene in several populations. The transcription factor AP-2a (TFAP2A), which is involved in regulating mid-face development and upper lip fusion, has ... [Abstract] [Full-text]

Articles on Cleft Palate published 28 June 2011:

Novel polymorphic AluYb8 insertion in the WNK1 gene is associated with blood pressure variation in Europeans.   Hum Mutat, 32(7): 806-14.

Mutations in WNK1 and WNK4 cause familial hypertension, the Gordon syndrome. WNK1 and WNK4 conserved noncoding regions were targeted to polymorphism screening using DHPLC and DGGE. The scan identified an undescribed polymorphic AluYb8 insertion in WNK1 intron 10. Screening in primates revealed that this Alu-insertion has probably occurred in human lineage. Genotyping in 18 populations from Europe, Asia, and Africa (n = 854) indicated an expansion of the WNK1 AluYb8 bearing chromosomes out of ... [Abstract] [Full-text]

Articles on Cleft Palate published 23 June 2011:

Microdeletion 20p12.3 involving BMP2 contributes to syndromic forms of cleft palate.   Am J Med Genet A, 155(7): 1646-53.

Orofacial clefts of the lip and/or palate comprise one of the most common craniofacial birth defects in humans. Though a majority of cleft lip and/or cleft palate (CL/P) occurs as isolated congenital anomalies, there exist a large number of Mendelian disorders in which orofacial clefting is part of the clinical phenotype. Here we report on two individuals and one multi-generational family with microdeletions at 20p12.3 that include the bone morphogenetic protein 2 (BMP2) gene. In two propositi ... [Abstract] [Full-text]

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