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 reduced muscarinic agonist-induced Kv7-current sup

5 DHEAS selectively increased the beta-cell mRNA expressio

6 DHEAS significantly increased ACh release above the pre-

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

8 DHEAS, progesterone, luteinizing hormone, testosterone,

9 DHEAS-treated Kv7.2 homomeric currents became resistant

10 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

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

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

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

14 /dL) and low or low-normal corticotropin and DHEAS levels.

15 measurement of cortisol, corticotropin, and DHEAS.

16 A linear relationship between DeltaR(ct) and DHEAS concentration was verified in the range from 10.0

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

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

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

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

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

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

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

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

25 ction in mean plasma levels of estradiol and DHEAS during and towards the end of chemotherapy (p-valu

26 two combined steroids, we infer that PS and DHEAS act through shared or overlapping binding sites.

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

28 resistin were higher, while ghrelin, T3, and DHEAS were lower, in adolescents with TB vs healthy cont

29 ion of a selective Kv7 inhibitor, XE991, and DHEAS eliminated analgesic effects of DHEAS in late phas

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

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

32 Because DHEAS correlated well with BT and considerably less well

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

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

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

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

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

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

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

40 bel-free impedimetric immunosensor to detect DHEAS, which was based on the modification of an oxidize

41 curacy, stability, and specificity to detect DHEAS.

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

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

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

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

46 al models predicted a novel binding site for DHEAS in the cytoplasmic domain of Kv7 subunits.

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

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

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

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

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

52 .51, 3.09); at 7 y, obese children with high DHEAS were fatter and more centrally obese than their co

53 However, DHEAS per se did not alter the voltage dependence of the

54 h significant association between decline in DHEAS levels and acute onset of CRCI at 6 weeks from bas

55 , OGTT results and HOMA-IR), hormone levels (DHEAS, SHBG, total and free testosterone and FAI), lipid

56 5 ug/dL), high corticotropin levels, and low DHEAS levels.

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

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

59 n the early diagnosis of pACC and to monitor DHEAS levels in other adrenal pathologies.

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

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

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

63 Furthermore, in vivo administration of DHEAS in mice of both sexes reduced late phase pain resp

64 Administration of DHEAS in vivo alleviated inflammatory pain in rodents.

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

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

67 1, and DHEAS eliminated analgesic effects of DHEAS in late phase responses in the formalin paw test.

68 7.2(H558C), resulted in a loss of effects of DHEAS on muscarinic Kv7 current suppression.

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

70 Treatment with precursors of DHEAS reduced opioid self-administration in zebrafish in

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

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

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

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

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

76 E/AuNPs-ARG/IgM was confirmed by quantifying DHEAS in real patient plasma samples, with results that

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

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

79 This enabled us to study DHEAS in clinical serum samples with several advantages

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

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

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

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

84 otropin, and dehydroepiandrosterone sulfate (DHEAS) are used to diagnose adrenal insufficiency.

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

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

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

88 teroids like dehydroepiandrosterone sulfate (DHEAS) down to 1.3 uM with no loss in binding affinity c

89 report that dehydroepiandrosterone sulfate (DHEAS) is an endogenous Kv7 channel modulator that atten

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

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

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

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

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

95 roduction of dehydroepiandrosterone sulfate (DHEAS), whose detection in serum or plasma can be effect

96 increase in dehydroepiandrosterone sulfate (DHEAS).

97 ate (PS) and dehydroepiandrosterone sulfate (DHEAS).

98 eurosteroid, dehydroepiandrosterone sulfate (DHEAS).

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

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

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

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

103 hydroepiandrosterone (DHEA) and its sulfate, DHEAS, are the major adrenal androgen precursors, but th

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

105 This study demonstrates that DHEAS, an endogenous steroid hormone, is a novel Kv7 cha

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

107 Collectively, these results suggest that DHEAS attenuates M-current suppression by stabilizing PI

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

109 The DHEAS detection principle was based on the variation of

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

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

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

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

114 uggests that the hormonal pathway related to DHEAS may be implicated in acute CRCI for breast cancer

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

116 ical understanding of the pathway from which DHEAS may correlate with cognitive dysfunction and its i

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

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

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

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