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1 eural tube defects (NTDs), known as diabetic embryopathy.
2 e implicated in the pathogenesis of diabetic embryopathy.
3 K)1/2 activation is associated with diabetic embryopathy.
4 e helping to define nongenetic mechanisms of embryopathy.
5 a key role in the malformations of diabetic embryopathy.
6 f the malformations associated with diabetic embryopathy.
7 cating cellular organelle stress in diabetic embryopathy.
8 ations (22 spontaneous abortions, 2 warfarin embryopathies, 1 stillbirth, 1 ventricular septal defect
9 s responsible for the occurrence of diabetic embryopathy, a spectrum of birth defects that includes h
10 K1 and JNK2 are equally involved in diabetic embryopathy and that the oxidative stress-JNK1/2-caspase
11 We established a model of type 2 diabetic embryopathy by feeding 4-week-old female mice a high-fat
17 sufficiency in this murine model of diabetic embryopathy is associated with caudal but not cranial NT
18 fficulties associated with studying diabetic embryopathy is the rarity of individual malformations.
20 ace and fingers, known as the anticonvulsant embryopathy, is increased in infants exposed to anticonv
22 Previous studies have shown that diabetic embryopathy results from impaired expression of genes th
23 congenital abnormalities consistent with MTX embryopathy secondary to weekly low-dose MTX treatment.
24 fection by ZIKV may contribute to associated embryopathies through signaling crosstalk between develo
25 that OGT plays an important role in diabetic embryopathy via increasing protein O-GlcNAcylation, and
26 The combined frequency of anticonvulsant embryopathy was higher in 223 infants exposed to one ant
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