dysmorphogenesis

dys·mor·pho·gen·e·sis

(dis'mōr-fō-jen'ĕ-sis),
The process of abnormal tissue formation.
[dys- + G. morphē, form, + genesis, production]

dysmorphogenesis

[dis′môrfōjen′əsis]
the development of ill-shaped or otherwise malformed body structures.

dys·mor·pho·gen·e·sis

(dis'mōr-fō-jen'ĕ-sis)
The process of abnormal tissue formation.
[dys- + G. morphē, form, + genesis, production]

dysmorphogenesis

Severe abnormality of body development caused by influences operating at an early stage of fetal growth. Monstrous maldevelopment (TERATOGENESIS).

dysmorphogenesis

giving rise to dysmorphism.
References in periodicals archive ?
Nkx2-5 is genetically upstream of multiple genes essential for heart development; 33 heterozygous loss-of-function mutations in this gene have been reported to cause heart malformations in humans, including conduction delay and atrial septal dysmorphogenesis (Biben et al.
Vascular malformations are congenital lesions of vascular dysmorphogenesis, are always present at birth, and enlarge in proportion to the growth of the child.
Animal-model-causes of windowing-induced dysmorphogenesis (neural-tube defects and early amnion deficit spectrum) in chicken embryos.
Evidence suggests that GC teratogenicity is a result of direct action on the embryo, which triggers a characteristic pattern of dysmorphogenesis via the biochemical and GC-mediated anti-inflammatory pathway (Kay et al.
We observed similar patterns of dysmorphogenesis and progressive loss of renal function at postnatal weeks 7 and 52 in the offspring of pregnant C57 but not D2N mice gavaged with 0.
In a number of murine models, overexpression of VEGF results in dysmorphogenesis, and underexpression of VEGF or neutralization of VEGF results in poor septal formation and emphysematous changes (Gerber et al.
In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces genital dysmorphogenesis in the female rat.
Controlled exposure to UV radiation has produced amphibian dysmorphogenesis (Ankley et al.
Similarly, diazinon has been shown to disrupt neurodevelopment in aquatic species (45,46) and elicits dysmorphogenesis in sea urchins during the phase in which neurotrophic factors control development (47).
By 5 days after fertilization, TCDD-exposed fish exhibited gross dysmorphogenesis in cranio-facial and vertebral development.
Importantly, just like the mammalian CNS, the sea urchin expresses nAChRs that are linked to cell replication, differentiation, and apoptosis; so in this species, xenobiotic effects on cholinergic signaling are reflected by easily observable dysmorphogenesis, whereas comparable effects in the developing brain tend to elicit more subtle alterations that entail biochemical and functional assessments (1-3,39,42-47,49).
In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)induces genital dysmorphogenesis in the female rat.