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1 ylthiocarbamide and P = 3.96 x 10-19 for 6-n-propylthiouracil).
2 s (thiamazole [methimazole], carbimazole, or propylthiouracil).
3 nvironmental trigger is the antithyroid drug propylthiouracil.
4 ecially following exposure to hydralazine or propylthiouracil.
5 thyroidectomy and subsequent treatment with propylthiouracil.
6 hydralazine and 3 (10%) had been exposed to propylthiouracil.
7 reaction is insensitive to inhibition by 6-n-propylthiouracil.
8 ds contained low Km D2 activity resistant to propylthiouracil (1 mM) or to inactivation by N-bromoace
9 restriction, we modeled the binding mode of propylthiouracil, a weak inhibitor of CYB5R3 (IC50 = app
10 5% CI, 6.4%-10.7%) of patients who initiated propylthiouracil and 6.3% (46 of 727; 95% CI, 4.6%-8.1%)
11 f the mutants to the selective D1 inhibitors propylthiouracil and aurothioglucose were unaltered.
16 rge to hospice between patients treated with propylthiouracil and those treated with methimazole, ass
17 ch as low K(m) (T(4)), 1.3 nm, resistance to propylthiouracil, and a short half-life ( approximately
18 uorescence pattern (pANCA) when treated with propylthiouracil, and changed back to anti-PR3 antibodie
20 , after the induction of hypothyroidism with propylthiouracil, and in response to T(3) administration
21 d the prevalence of exposure to hydralazine, propylthiouracil, and other drugs previously implicated
22 ve been reports suggesting that hydralazine, propylthiouracil, and several other drugs may cause some
24 ediated bitterness of phenylthiocarbamide or propylthiouracil, but now it encompasses additional phen
27 days of maternal goitrogen treatment (10 ppm propylthiouracil) during the perinatal period (GD19-PN2)
28 ts that treatment with either hydralazine or propylthiouracil is associated with ANCA-positive vascul
29 l of 1383 patients (656 [47.4%] treated with propylthiouracil; mean [SD] age, 45 [16] years; 473 wome
30 ypical tastants (phenylthiocarbamide and 6-n-propylthiouracil, NaCl, sucrose, monopotassium glutamate
32 , treatment with anti-thyroid hormone drugs (propylthiouracil or methimazole) completely rescues SMRT
37 variation in bitter taste perception of 6-n-propylthiouracil (PROP) and structurally similar compoun
38 Taste blindness to the bitterness of 6-n-propylthiouracil (PROP) has been associated with increas
39 y to taste phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PROP) is a polymorphic trait mediated
40 bitter taste of phenylthiocarbamide and 6-n-propylthiouracil (PROP) is a well-studied human trait.
41 tion in sensitivity to the bitterness of 6-n-propylthiouracil (PROP) is thought to play a role in the
42 HCl, caffeine, sucrose octaacetate (SOA) and propylthiouracil (PROP) solutions were examined in 1457
45 on of late, namely hydralazine, minocycline, propylthiouracil (PTU) and levamisole-adulterated cocain
46 duced in adult rats by treatment with 0.025% propylthiouracil (PTU) for 6 weeks (PTU-S) and 1 year (P
47 sed to the model thyroid hormone suppressant propylthiouracil (PTU) from < 1 to 30 days post hatch.
50 was induced by administration of 3 or 10 ppm propylthiouracil (PTU) to pregnant and lactating dams vi
51 slow skeletal TnI (ssTnI), were treated with propylthiouracil (PTU) to revert MHC expression from adu
52 3)) and thyroxine (T(4))) or inhibitors (6-N-propylthiouracil (PTU), Tetrabromobisphenol A (TBBPA)) o
56 rat hearts containing alpha-MHC isoform and propylthiouracil (PTU)-treated rat hearts containing bet
60 the synthesis of triiodothyronine (T3) with propylthiouracil rescued pressure overload-induced hyper
61 tion of TH by treating Thrb(PV/PV) mice with propylthiouracil (Thrb(PV/PV)-PTU mice) and compared the
64 , we validated two new potent derivatives of propylthiouracil, ZINC05626394 (IC50 = 10.81 muM) and ZI