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1 tive thyroid hormone synthesis, resulting in congenital hypothyroidism.
2 tial therapeutic targets in the treatment of congenital hypothyroidism.
3 UOX expression and the molecular genetics of congenital hypothyroidism.
4 ons may induce constitutive inactivation and congenital hypothyroidism.
5 lities associated with human prematurity and congenital hypothyroidism.
6 syndrome and death, and 1 case of transient congenital hypothyroidism.
7 e sequencing data in patients suffering from congenital hypothyroidism.
8 humans is associated with the development of congenital hypothyroidism.
11 in differentiating transient from permanent congenital hypothyroidism and predicting the response of
13 In a number of human kindreds suffering from congenital hypothyroidism, and in the cog congenital goi
14 plicated in glucose/galactose malabsorption, congenital hypothyroidism, Bartter's syndrome, epilepsy,
20 t result in a non-functional protein lead to congenital hypothyroidism due to I(-) transport defect (
24 have linked mutations in the ChEL domain to congenital hypothyroidism in humans and rodents; these m
26 tosomal recessive trait, deficient Tg causes congenital hypothyroidism in newborns that, if untreated
27 The Tg-G2320R mutation is responsible for congenital hypothyroidism in rdw/rdw rats, in which a la
30 20R (G221R in NLGN) mutation responsible for congenital hypothyroidism into NLGN3, we show that mutat
34 ily used to locate ectopic thyroid tissue in congenital hypothyroidism or to detect defects in iodine
37 roglobulin can result in autosomal recessive congenital hypothyroidism with deficient thyroglobulin.