ライフサイエンスコーパス: active vitamin

1 All-trans-retinoic acid (ATRA) is an active vitamin A derivative known to modulate a number o

2 Retinoic acid (RA), an active vitamin A derivative, is essential for mammalian

3 g a CD133 peptide attached to an osmotically active vitamin B(6)-coupled polydixylitol vector (VPX-CD

4 kers were found for riboflavin, vitamin B-6, active vitamin B-12 (holotranscobalamin), and betaine.

5 ammalian enzymes that utilise a biologically active vitamin B-12 derivative.

6 scobalamin 2 (TCN2), which is referred to as active vitamin B-12.

7 As confirmed by UHPLC-MS, the active vitamin B12 could be separated from pseudovitamin

8 and validated for the determination of human active vitamin B12 in cell extracts of Propionibacterium

9 form, adding complexity to our assessment of active vitamin B12 in the environment.

10 A nutritionally relevant amount of active vitamin B12 was produced by P. freudenreichii in

11 ts superiority to the MBA in determining the active vitamin B12.

12 sma folate, B12, and pyridoxal 5'-phosphate (active vitamin B6) levels, along with other potential de

13 ortant cofactor pyridoxal-5'-phosphate (PLP, active vitamin B6) through its complexation with P6C.

14 ents with PSC and the effects of exposure to active vitamin D (1,25[OH]2D3) on expression of CD28.

15 s considered when there still was a need for active vitamin D 1 year after surgery.

16 thyroidism varied between 14.5% (calcium and active vitamin D 1 year postsurgery) to 28.5% (calcium a

17 1 year postsurgery) to 28.5% (calcium and/or active vitamin D 6 months postsurgery) depending on the

18 ated hormone-controlled system that involves active vitamin D [1,25(OH)(2)D], which can elicit calciu

19 D receptor (VDR), and the ability to produce active vitamin D [1,25(OH)2D, regulated by Cyp27b1] regu

20 that encodes the primary catabolic enzyme of active vitamin D [25(OH)D-24-hydroxylase encoded by CYP2

21 ism by which local conversion of inactive to active vitamin D alters immune function in the lung.

22 ed more commonly in patients treated with an active vitamin D analog (204/390 patients) than control

23 We found that treatment with active vitamin D analog paricalcitol prevented mouse bod

24 Thus, active vitamin D analogs may further reduce proteinuria

25 We aimed to address whether active vitamin D analogs reduce residual proteinuria.

26 Active vitamin D analogs reduced proteinuria (weighted m

27 tamin D, as well as increases in circulating active vitamin D and Ca(2+) and in bone formation in mic

28 Active vitamin D and calcium were progressively reduced,

29 Because serum levels of active vitamin D are greatly increased upon genetic abla

30 oportion of patients who reduced the dose of active vitamin D at Month 6 (31% vs. 10% in the placebo

31 Treatment with high-dose oral calcium and active vitamin D does not provide adequate or consistent

32 ptimisation period, during which calcium and active vitamin D doses were adjusted to achieve consiste

33 erum 1,25(OH)(2)D levels, and hence, reduces active vitamin D drugs.Clinical Trial Registry: This stu

34 f the prohormone 25-hydroxyvitamin D and the active vitamin D hormone 1, 25-dihydroxyvitamin D.

35 berculosis H37Ra and then activated with the active vitamin D hormone 1,25-dihydroxyvitamin D(3) (1,2

36 n correlated with both circulating levels of active vitamin D hormone and in vitro measures of gene e

37 droxylase, which functions to metabolize the active vitamin D in cells.

38 m in chronic kidney failure with calcium and active vitamin D is potentially limited by hypercalcemia

39 d with increased MS susceptibility and lower active vitamin D levels.

40 triol (1alpha,25-dihydroxyvitamin D3) is the active vitamin D metabolite and mediates immunological f

41 Notably, administration of the active vitamin D metabolite calcitriol reversed all thes

42 ncert with parathyroid hormone (PTH) and the active vitamin D metabolite, 1,25(OH)(2) vitamin D (1,25

43 The active vitamin D metabolite, 1,25-dihydroxyvitamin D, ac

44 of 1,25-dihydroxyvitamin D [1,25(OH)2D], the active vitamin D metabolite, from 25-hydroxyvitamin D [2

45 nal treatment with phosphate supplements and active vitamin D metabolites (such as calcitriol) improv

46 was defined as treatment with calcium and/or active vitamin D more than 1 year after surgery.

47 tes mellitus, we investigated the effects of active vitamin D on macrophage cholesterol deposition.

48 poparathyroidism was defined as the need for active vitamin D postoperatively, whereas permanent hypo

49 5 hydroxylase that converts vitamin D3 to an active vitamin D receptor ligand; P=1.4x10(-5)).

50 se activities to an unusual but functionally active vitamin D response element and to several potenti

51 which include 242 patients who were given an active vitamin D sterol.

52 al insufficiency (CCr, 25 to 60 ml/min), the active vitamin D sterols calcitriol or alfacalcidol [1 a

53 therapy with calcium, phosphate binders, and active vitamin D sterols, were treated in this 18-wk, do

54 reby increasing the safety of treatment with active vitamin D sterols.

55 ular epithelial cells are the major sites of active vitamin D synthesis, little is known about the ro

56 Active vitamin D that is generated by lung epithelium le

57 tion increased over time, whereas the use of active vitamin D was unchanged.

58 line in their daily dose of oral calcium and active vitamin D while maintaining a serum calcium conce

59 hypoparathyroidism, defined as the need for active vitamin D with or without calcium supplementation

60 We show in this article that biologically active vitamin D(3) [1,25(OH)(2)-D(3)] significantly dow

61 We show in this article that biologically active vitamin D(3) [1,25(OH)(2)-D(3)] significantly dow

62 the preclinical model of AD, induced by the active vitamin D(3) analog MC903 (calcipotriol), NTCI su

63 induction of Sult2A1 mRNAs by the hormonally active vitamin D(3) and the catatoxic synthetic steroid

64 nphotochemical steps to achieve biologically active vitamin D(3) has been established from ex vivo da

65 Hormonally active vitamin D(3)-1,25-dihydroxyvitamin D(3) (1,25D3)-

66 Indeed, we found that small doses of active vitamin D, 1alpha,25-dihydroxyvitamin D3 (1,25D3)

67 DL cholesterol, and use of aspirin, statins, active vitamin D, and antihypertensive medications, in f

68 lpha-hydroxylase, augments the production of active vitamin D, and synergizes with vitamin D to incre

69 ting hydroxylase catalyzing the formation of active vitamin D, as well as increases in circulating ac

70 Active vitamin D, generated locally in tissues, is impor

71 Only KTRs not receiving active vitamin D, poor 1,25D status predicted the worse

72 al therapy, consisting of oral phosphate and active vitamin D, versus switching to burosumab, a fully

73 clude that primary epithelial cells generate active vitamin D, which then influences the expression o

74 uent doses of oral phosphate supplements and active vitamin D, which was of limited efficiency and as

75 te that human endothelia are able to produce active vitamin D.

76 BP) regulates concentrations of biologically active vitamin D.

77 lphabeta(ep-/-)) or a topical application of active vitamin D3 (VD3) and/or all-trans retinoic acid (

78 c renal failure, where concentrations of the active vitamin D3 metabolite, 1alpha,25-dihydroxyvitamin

79 045), and suggested an increased risk in the active vitamin group (P =.09).

80 a functional vitamin K cycle to produce the active vitamin K cofactor for the gamma-carboxylase whic

81 e cycle reduces vitamin K 2,3-epoxide to the active vitamin K hydroquinone cofactor.

82 arin-treated zebrafish, which have decreased active vitamin K, display similar vascular degeneration

83 K-dependent carboxylase modifies and renders active vitamin K-dependent proteins involved in hemostas

84 is a key regulatory protein in synthesis of active vitamin K-dependent proteins.

85 Patients receiving active vitamin treatment had similar risk for the compos