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 ?
1-3] In general, the FA phenotype is characterised by a broad spectrum of congenital anomalies, principally involving growth, skin pigmentation and dysmorphogenesis of the skeletal, cardiovascular, genito-urinary, gastrointestinal and central nervous systems (CNS).
150) With respect to peroxisomal dysmorphogenesis in humans, only three patients have been identified with a different defect in two proteins involved in the proliferation and division of peroxisomes.
In utero and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induces genital dysmorphogenesis in the female rat.
Hyperglycemia-induced embryonic dysmorphogenesis correlates with genomic DNA mutation frequency in vitro and in vivo .
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.
The present study was undertaken to determine the dysmorphogenesis effects of AgNPs on fetal development after maternal exposure on gestational days (GD) 4-15 in mice.
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.
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.