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An experimental study was designed to investigate the effects of the lipid or water soluble subfractions of meconium on the intestines of gastroschisis in a chick model.
The present study was designed to establish a chick model for the mechanisms of SM on neurobehavioral teratogenicity, free of confounds related to mammalian maternal effects.
The present study was designed to evaluate the suitability of a chick model for phthalate DEHP teratogenicity and neurobehavioral teratogenicity, a model which is simple and devoid of potential confounding factors such as maternal toxicity, maternal-fetal unit and maternal-neonatal interactions; major findings were confirmed in the DBP study.
Here, we demonstrated that embryonic hypoxia results in cardiac disease at both late embryonic stages and adulthood in a chick model.
The goal of this work was to quantify hypoxia-induced morphological and cellular changes in a chick model, with the hypothesis that malformations are generated by changes in normal cellular processes.
We found that the majority of shape variation in Twsg1 +/− mouse embryos with intrauterine exposure to a low dose of ATRA was associated with narrowing of the midface as seen in the human microforms (Roessler et al., 1996), Noggin-null mice (Lana-Elola et al., 2011) and in a chick model of HPE (Marcucio et al., 2005; Young et al., 2010).
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This report presents a dietary chick model of severe hyperhomocysteinemia as a superior alternative to the CBS-knockout mouse [ 7] for study of connective tissue abnormalities.
Besides, a different chick model system by in vivo chick embryonic CAM assay showed that the number of blood vessels gradually decreased with increasing concentrations of ellagic acid accompanied by VEGF stimulation (Fig. 3c).
Using an established chick model, the effectiveness of sevelamer in preventing the apparent absorption of liberated phytate phosphate during active vitamin D use was investigated in two separate experiments.
Finally, we were able to phenocopy the mouse phenotype in the chick model using a VEGFR2 inhibitor.
In this article, we use the chick model system to provide a global view on how RA influences organ position at different levels along the AP axis.
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