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Lipomas are considered to be rare congenital benign malformations resulting from developmental aberrations involving the meninx primitiva.
These structures resemble capillary malformations resulting from local overexpression of VEGF [20], [21] suggesting that VEGF may be overexpressed in the skin of c-GVHD patients as it is in the skin of patients with SSc [22].
Orofacial malformations resulting from genetic and/or environmental causes are frequent human birth defects yet their etiology is often unclear because of insufficient information concerning the molecular, cellular and morphogenetic processes responsible for normal facial development.
Malformations resulting from exposure to 1.5 nm MES-AuNPs included the jaw, eyes, snout, heart, and fins.
By contrast, axis malformations resulting from early En2 activation are equally observed with wild-type and mutant proteins and are insensitive to antibody treatment.
Consequently, the phenotypes resulting from loss of gene function through mutation can be compared to malformations resulting from embryonic exposure to contaminants.
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Although some cortical malformations result from environmental insults during cortical development in utero, genetic factors are increasingly recognized as primary pathogenic factors across the entire spectrum of malformations.
Some congenital malformations result from genetic defects, others from environmental factors.
The malformations resulted from infection of the dams in summer or autumn 2011 and transplacental transmission.
Other researchers have not found such strong relationships between agriculture and reproductive abnormalities, and they argue that observed gonadal malformations result from natural developmental processes.
These experimental findings suggest that atrazine-induced gonadal malformations result from the depletion of androgens and production of estrogens, perhaps subsequent to the induction of aromatase by atrazine, a mechanism established in fish, amphibians, reptiles, and mammals (rodents and humans).
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