ライフサイエンスコーパス: hyperthyroid

1 pe and Tshr-knockout mice that were rendered hyperthyroid.

2 NA occurred when euthyroid animals were made hyperthyroid.

3 .7-fold increase in protein content while in hyperthyroid aged rats, the increase of THRP mRNA was on

4 36% developed thyroid dysfunction: 19 became hyperthyroid and 14 hypothyroid.

5 s (26 months old) were studied at euthyroid, hyperthyroid and hypothyroid conditions.

6 or subclinical thyroid dysfunction (127 were hyperthyroid, and 168 were hypothyroid).

7 AF incidence was 78% in hypothyroid, 67% in hyperthyroid, and the duration of induced AF was also lo

8 esonance spectroscopy, was reduced by 59% in hyperthyroid animals (0.0022 +/- 0.0002 versus 0.0055 +/

9 ficantly reduced the hypertrophy observed in hyperthyroid animals (100 +/- 20 versus 200 +/- 30 mg; P

10 alpha, are greatly increased in the liver of hyperthyroid animals.

11 This study shows that hyperthyroid compared to euthyroid cats have higher seru

12 undance is increased 40-fold in the liver of hyperthyroid compared with hypothyroid rats.

13 iologically relevant concentrations but that hyperthyroid conditions are required to suppress express

14 4-83.17) when compared with a small group of hyperthyroid controls (p=5.04 x 10(-4)).

15 essing all other associations of subclinical hyperthyroid disease and adverse clinical outcomes or tr

16 ce in the United States for most adults with hyperthyroid disease.

17 of the stimulating variety are the cause of hyperthyroid Graves disease.

18 an increase the metabolic flexibility of the hyperthyroid heart and reduce the level of hypertrophy t

19 f in vivo pyruvate dehydrogenase flux in the hyperthyroid heart and to establish whether modulation o

20 that inhibition of glucose oxidation in the hyperthyroid heart in vivo is mediated by pyruvate dehyd

21 of which was significantly increased in the hyperthyroid heart.

22 iac hypertrophy models with hypothyroid- and hyperthyroid-like changes in the TH target genes, alpha-

23 yte TRbeta1 was upregulated in models with a hyperthyroid-like phenotype, TH (triiodothyronine, T3),

24 We found that hyperthyroid mice lacking TSHR had greater bone loss and

25 In hyperthyroid mice, this synthetic circuit sensed patholo

26 ge in cultured cells and in tissues of young hyperthyroid mice.

27 xpressed a biotinylated TRbeta1 in hypo- and hyperthyroid mouse livers, used ChIP-seq to identify gen

28 60 of these cats had a euthyroid (n = 23) or hyperthyroid (n = 37) status, all of which were used in

29 into hypothyroid (N=9), euthyroid (N=9), and hyperthyroid (N=9) groups.

30 Hyperthyroid non-Hispanic black women had higher odds of

31 genous T3 that rendered the animals slightly hyperthyroid, only induction of hepatic CYP4A2 mRNA by D

32 an (131)I tracer administered to small-pool hyperthyroid patients (n = 9) not receiving ATDs (off AT

33 evels averaged 158 ng/100 ml in 11 untreated hyperthyroid patients and 84 ng/100 ml in 15 untreated p

34 uptake ratio of > or = 1 was found in 15% of hyperthyroid patients and was associated with a near 50%

35 for thyroid uptake of 123I in euthyroid and hyperthyroid patients in Boston have remained stable for

36 A total of 35 593 hyperthyroid patients treated between 1946 and 1964 in t

37 ical variations in the yearly values for the hyperthyroid patients were evident but not clinically im

38 e obtained in 671 euthyroid patients and 274 hyperthyroid patients, of which 233 patients had a diffu

39 In 433 hyperthyroid patients, the success of 131I therapy was c

40 significant improvement for the treatment of hyperthyroid patients.

41 as an index of thyroidal iodide retention in hyperthyroid patients.

42 (1979-83) and the later years (1988-94) for hyperthyroid patients.

43 etermine the levels of these proteins in the hyperthyroid primate heart and mediate, in part, the obs

44 tent and accumulation of MDA-bound proteins, hyperthyroid rats and hypothyroid rats were compared to

45 ac systolic and diastolic functions, whereas hyperthyroid rats exhibited cardiac hypertrophy and incr

46 bout 2.5-fold slower than in myocardium from hyperthyroid rats expressing only the alpha MHC isoform,

47 in hypothyroid rats and increased 6-fold in hyperthyroid rats.

48 Pase and phospholamban mRNA increased in the hyperthyroid state, and alpha-MHC mRNA appeared de novo,

49 n rats administered exogenous T3 to attain a hyperthyroid state, induction of the three isozymes of C

50 mulating hormone (TSH), which is low in most hyperthyroid states, directly affects the skeleton.

51 ths of age during euthyroid, hypothyroid and hyperthyroid states.

52 nd of treatment, hypothyroid, euthyroid, and hyperthyroid status was confirmed.

53 ed T3-regulated gene expression of hypo- and hyperthyroid transgenic mice.

54 HR had greater bone loss and resorption than hyperthyroid wild-type mice, thereby demonstrating that