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At least 1,351 records · Page 75Linked to original sources
PubMed1992

Expression of Hox 2.1 protein in restricted populations of neural crest cells and pharyngeal ectoderm.

A polyclonal antibody, alpha Hox 2.1a, was used to localize Hox 2.1 protein in presumptive neural crest cells and nodose ganglion of 8.5-10.0 day p.c. mouse embryos. The following results were obtained: (1) The nodose placode, in its epithelial state, first expresses Hox 2.1 protein at 9.0 d.p.c. By 9.5 d.p.c. presumptive migrating neuroblasts between the nodose placode and ganglion primordium also express Hox 2.1 protein. (2) At 9.5 d.p.c., presumptive crest cells lateral to the cephalic cardinal vein and within pharyngeal arches 4 and 6 are immunoreactive for alpha Hox 2.1a. In the arch 6 region, positive cells extend medially to a mesenchymal cell population on the lateral aspect of the foregut wall. (3) At 10.0 d.p.c., Hox 2.1 protein expression in putative crest cells is restricted to the arch 6 cell population. A similar staining pattern is seen using alpha Hox 2.1a with chick embryos. Comparison with the chicken embryo suggests that the Hox 2.1 positive cells in the pharyngeal arch and those on the lateral aspect of the foregut in the mouse embryo correspond to the caudalmost subpopulation of the circumpharyngeal crest (Kuratani and Kirby: Am. J. Anat. 191:215-227, 1991; Anat. Rec. 234:263-280, 1992). These results are consistent with a role for Hox 2.1 in pattern formation in the caudalmost region of the vertebrate head.

Animals↗
PubMed1981

An autosomal recessive ectodermal dysplasia syndrome of hypotrichosis, onychodysplasia, hyperkeratosis, kyphoscoliosis, catartact, and other manifestations.

We describe a 20-year-old woman with generalized trichodysplasia, dry skin with scaling, hyperchromic spots on limbs, hyperkeratosis (particularly intense on soles), dermatoglyphic abnormalities, onychodysplasia, shortness of stature, kyphoscoliosis, unusual facial appearance, minor malformations of limbs, bilateral nuclear cataract, narrow palpebral fissures, entropion, trichiasis, etc. The condition is probably due to an autosomal recessive gene. The patient is the only affected member in a sibship of four whose parents are second cousins.

Abnormalities, Multiple↗
PubMed1983

AREDYLD: a syndrome combining an acrorenal field defect, ectodermal dysplasia, lipoatrophic diabetes, and other manifestations.

A daughter of second cousins is described as having lipoatrophic diabetes, unusual facial appearance, generalized hypotrichosis, two natal teeth with enamel dysplasia, eruption of four dysplastic deciduous teeth, absence of permanent dentition, low birth weight, short stature, lumbar scoliosis, renal alterations, aplasia of a breast and hypoplasia of the other, hypoplastic and hypopigmented areolae with diffuse limits, hyperostosis of the cranial vault, metacarpal hypoplasias, difficulty of grasping with the left hand, exertional dyspnea, absence of DIP extension and flexion creases, dermatoglyphic alterations, and other anomalies. Her sister, dead at 1 1/2 years, had had some manifestations of the condition; seven sibs are normal. It is more likely that the whole clinical picture represents a single syndrome rather than homozygosity of different autosomal-recessive genes.

Abnormalities, Multiple↗
PubMed1986

An unusual case of ectodermal dysplasia.

The syndrome was characterized by striking hypoplasia of nails, malformations of hands and feet, curly hair, small lower teeth and seizures. There were no similarly affected relatives. Death occurred at 31 months with the patient apparently in status epilepticus with terminal hepatorenal syndrome.

Child, Preschool↗
PubMed1988

Genitourinary anomalies are a component manifestation in the ectodermal dysplasia, ectrodactyly, cleft lip/palate (EEC) syndrome.

Here we report on 13 individuals with the EEC syndrome from a single craniofacial clinic population. Eight of 13 underwent genitourinary (GU) evaluation; all had abnormal findings. Seven had anomalies of the urinary tract, and 3 had genital anomalies. To our knowledge, this is the first report of GU evaluation of the majority of EEC patients from a single clinic population. Results support the suggestion that GU anomalies are a major component of the EEC syndrome. Genitourinary evaluation of all EEC patients and their first degree relatives seems indicated. The abnormal findings observed to date suggest variable expression of an autosomal dominant gene.

Abnormalities, Multiple↗
PubMed1994

Aplasia cutis congenita with epibulbar dermoids: further evidence for syndromic identity of the ocular ectodermal syndrome.

We have investigated 2 young South African girls with aplasia cutis congenita, epibulbar dermoids, and strabismus. This unique association of anomalies was first documented in two unrelated boys by Toriello et al. [1993: Am. J. Med. Genet. 45:764-766]. Our clinical and histological findings are markedly similar, and we think this to be the second report of individuals with this rare syndrome.

Adult↗