ライフサイエンスコーパス: DHEAS

1 DHEAS 10(-6) M significantly increased neuron survival b

2 DHEAS concentrations were similar between girls (30.3 +/

3 DHEAS is identical to PS except that it contains a carbo

4 DHEAS selectively increased the beta-cell mRNA expressio

5 DHEAS significantly increased ACh release above the pre-

6 DHEAS, E(2)17betaG, and methotrexate were transported wi

7 4.61 [7.97] vs 20.57 [4.9] nmol/L; P = .04), DHEAS (3.63 [2.19] vs 2.64 [1.49] microg/mL; P = .02), L

8 ne decreased by 6.0% (95% CI: -8.4%, -3.6%), DHEAS decreased by 5.1% (95% CI: -9.6%, -0.4%), and the

9 However, certain M1 mutations affected DHEAS differently than PS.

10 Although DHEAS is a peroxisomal proliferator, it did not alter th

11 DHEA and DHEAS are found in brains from many species, and we have

12 ata indicate that pretreatment with DHEA and DHEAS at physiologically relevant concentrations promote

13 lts confirm prior evidence that low DHEA and DHEAS can predict IHD in men.

14 ide evidence of mechanisms by which DHEA and DHEAS exert biological actions, show that they have spec

15 DHEA and DHEAS modulation of anoxia in embryonic neurons may be r

16 treated mice contained 10-fold more DHEA and DHEAS than did samples from unsupplemented mice, DHEAS a

17 ed if products of P450c17 activity, DHEA and DHEAS, regulated the motility and/or growth of neocortic

18 Supernatant from DHEA and DHEAS-exposed cultures was tested for 17beta-estradiol m

19 he only structural difference between PS and DHEAS, and second, the strongest chemical and steric eff

20 uding the previously reported metabolites as DHEAS, cortisol and androstenedione and extending that t

21 of sulfated and unsulfated steroids, such as DHEAS and allopregnanolone, act at distinct sites implie

22 Because DHEAS correlated well with BT and considerably less well

23 evidence was found of an association between DHEAS and risk of breast cancer in postmenopausal women.

24 hilean Cohort Study the associations between DHEAS and weight, BMI, waist circumference (WC), waist-t

25 ncurrent measurements of serum levels of BT, DHEAS, and IGF-1/GH together with detailed studies of th

26 neuron survival by 74% following anoxia, but DHEAS 10(-10) M decreased neuron survival after this ins

27 By contrast, DHEAS had no effect on Tau-1 axonal neurites but increas

28 , free testosterone, dehydroepiandrosterone (DHEAS), androstenedione, luteinizing hormone, and follic

29 rosterone (DHEA) and its sulfate derivative (DHEAS) are the most abundant steroids produced by the hu

30 ignificantly increases serum levels of DHEA, DHEAS, testosterone and estrone and substantially alters

31 dministration enhanced serum levels of DHEA, DHEAS, testosterone, and estrone, and regression analyse

32 isual Search tasks and serum levels of DHEA, DHEAS, testosterone, estrone, and cortisol were measured

33 -free medium, cultures were exposed to DHEA, DHEAS, or allopregnanolone (10(-10), 10(-8), or 10(-6) M

34 piandrosterone (DHEA), or its sulfated form (DHEAS), controls hyperglycemia in diabetic rodents witho

35 Although urine samples from DHEAS-treated mice contained 10-fold more DHEA and DHEAS

36 bese and obese children with normal and high DHEAS (>/=75th percentile) at 7 y.

37 etaG, the attenuation of this effect at high DHEAS concentrations and the lack of reciprocal promotio

38 Obese children had twice the risk of high DHEAS (OR: 2.16; 95% CI: 1.51, 3.09); at 7 y, obese chil

39 .51, 3.09); at 7 y, obese children with high DHEAS were fatter and more centrally obese than their co

40 S than did samples from unsupplemented mice, DHEAS administration did not affect body weight, life sp

41 ter co-application of the negative modulator DHEAS and the positive modulator allopregnanolone.

42 nhance the concentration of the neurosteroid DHEAS in rat brain.

43 e first to demonstrate that the neurosteroid DHEAS, a negative allosteric modulator of the GABAA rece

44 Based upon the stimulatory action of DHEAS on uptake of E(2)17betaG, the attenuation of this

45 er, the increases in brain concentrations of DHEAS and DHEA after injection of DHEAS i.p. were attenu

46 This effect of DHEAS on insulin secretion may contribute to the amelior

47 rations of DHEAS and DHEA after injection of DHEAS i.p. were attenuated by pretreatment with COUMATE.

48 ions and the lack of reciprocal promotion of DHEAS uptake by E(2)17betaG, a model involving nonrecipr

49 ssion and the consequent increased uptake of DHEAS and subsequent resistance to ADT, which, in turn,

50 S inhibition had broadly parallel effects on DHEAS, suggesting the two neurosteroids act through simi

51 nd the impact of SLCO2B1 expression level on DHEAS (dehydroepiandrosterone sulfate) uptake was evalua

52 ine, to test whether serum levels of DHEA or DHEAS could predict incident IHD over a 9-year interval.

53 alysis sample of 1,167 men, those with serum DHEAS in the lowest quartile at baseline (<1.6 microg/ml

54 co-endocrinological profiles (LH, FSH, SHBG, DHEAS, and testosterone levels) of men with early AGA an

55 These results suggest DHEAS rather than DHEA enhances brain cholinergic functi

56 es such as dehydroepiandrosterone 3-sulfate (DHEAS) and estrone 3-sulfate, glucuronides such as estra

57 he effect of dehydroepiandrosterone sulfate (DHEAS) administered i.p. on the release of acetylcholine

58 osterone and dehydroepiandrosterone sulfate (DHEAS) and subsequent risk of breast cancer in a case-co

59 tive steroid dehydroepiandrosterone sulfate (DHEAS) at 1 and 40 mg/kg caused dose-dependent increases

60 dicators and dehydroepiandrosterone sulfate (DHEAS) at 7 y of age and to evaluate the role of hormona

61 eased plasma dehydroepiandrosterone sulfate (DHEAS) concentrations by 88.2%, decreased plasma dehydro

62 and elevated dehydroepiandrosterone sulfate (DHEAS) levels, which supports a genetic basis for these

63 terone (BT), dehydroepiandrosterone sulfate (DHEAS), and the ratio of insulin-like growth factor 1 (I

64 enedione and dehydroepiandrosterone sulfate (DHEAS), averaged across the three menstrual cycle phases

65 ulin (SHBG), dehydroepiandrosterone sulfate (DHEAS), luteinizing hormone (LH), follicle-stimulating h

66 one sulfate, dehydroepiandrosterone sulfate (DHEAS), pregnanolone, and allopregnanolone, modulate ion

67 eurosteroid, dehydroepiandrosterone sulfate (DHEAS).

68 ostenedione, dehydroepiandrosterone sulfate (DHEAS)], sex hormone binding globulin (SHBG), and EOC ri

69 p were also given 25 microg/ml DHEA sulfate (DHEAS) in their drinking water.

70 However, mice produce DHEA and DHEA-sulfate (DHEAS) in the fetal brain.

71 hydroepiandrosterone (DHEA) and its sulfate (DHEAS) have been characterized as "protective" against i

72 -limiting in the functions measured and that DHEAS relates more indirectly to these functions.

73 We show that DHEAS enhanced glucose-stimulated insulin secretion when

74 f steroid exposure in vitro, suggesting that DHEAS did not directly activate the secretory processes.

75 as COUMATE interfere with the influx of the DHEAS anion into the brain.

76 n was expected to increase the amount of the DHEAS dose reaching the brain.

77 Thus, DHEAS directly affected the beta-cell to enhance glucose

78 Thus, DHEAS, as administered here, influenced neither cancer n

79 the intervention groups (all P<.01), whereas DHEAS and glucose levels were unchanged.

80 of mouse neocortical neurons in vitro, while DHEAS stimulates dendritic growth from those cells.

81 ere positively and similarly associated with DHEAS [ie, BMI, beta standardized regression coefficient

82 eight, obesity is positively associated with DHEAS at 7 y of age.

83 at SLCO2B1 expression levels correlated with DHEAS uptake by PC cells.