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1 exposure in pregnancy carries a high risk of embryopathy.
2 cating cellular organelle stress in diabetic embryopathy.
3 e implicated in the pathogenesis of diabetic embryopathy.
4 K)1/2 activation is associated with diabetic embryopathy.
5 e helping to define nongenetic mechanisms of embryopathy.
6  a key role in the malformations of diabetic embryopathy.
7 eural tube defects (NTDs), known as diabetic embryopathy.
8 f the malformations associated with diabetic embryopathy.
9 ations (22 spontaneous abortions, 2 warfarin embryopathies, 1 stillbirth, 1 ventricular septal defect
10 s responsible for the occurrence of diabetic embryopathy, a spectrum of birth defects that includes h
11 K1 and JNK2 are equally involved in diabetic embryopathy and that the oxidative stress-JNK1/2-caspase
12 among genes associated with RBS, thalidomide embryopathy, and other genetic limb reduction disorders,
13    We established a model of type 2 diabetic embryopathy by feeding 4-week-old female mice a high-fat
14  spectrum of malformations known as diabetic embryopathy (DE).
15 ndoplasmic reticulum (ER) stress in diabetic embryopathy has never been explored.
16                  Its involvement in diabetic embryopathy has not been established.
17 m (ER) stress, two causal events in diabetic embryopathy, has not been determined.
18 etformin effectively reduces type 2 diabetic embryopathy in a useful rodent model.
19  antithyroid drug use can cause drug-induced embryopathy in pregnancy, radioiodine therapy can exacer
20 sufficiency in this murine model of diabetic embryopathy is associated with caudal but not cranial NT
21 fficulties associated with studying diabetic embryopathy is the rarity of individual malformations.
22      Moreover, if susceptibility to diabetic embryopathy is variable in humans as well as in mice, it
23 ace and fingers, known as the anticonvulsant embryopathy, is increased in infants exposed to anticonv
24 nomalies and/or deafness) syndrome, diabetic embryopathy, other genetic variants, and FOXN1 deficienc
25                  This suggests that diabetic embryopathy results from impaired expression of genes re
26    Previous studies have shown that diabetic embryopathy results from impaired expression of genes th
27 congenital abnormalities consistent with MTX embryopathy secondary to weekly low-dose MTX treatment.
28 fection by ZIKV may contribute to associated embryopathies through signaling crosstalk between develo
29 that OGT plays an important role in diabetic embryopathy via increasing protein O-GlcNAcylation, and
30     The combined frequency of anticonvulsant embryopathy was higher in 223 infants exposed to one ant
31  apoptosis (causal events in type 1 diabetic embryopathy) were observed in embryos of DM dams.