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1 emia and inappropriately low serum levels of 1,25-dihydroxyvitamin D.
2 n of 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D.
3 one (PTH), insulin-like growth factor 1, and 1,25-dihydroxyvitamin D.
4 ne that catabolizes 25-hydroxy-vitamin D and 1,25-dihydroxyvitamin D.
5 y low but is highly induced by its substrate 1,25-dihydroxyvitamin D.
6 ceptors (VDRs), suggesting responsiveness to 1,25-dihydroxyvitamin D.
7 not affected by different concentrations of 1,25-dihydroxyvitamin D.
8 xyvitamin D and the active vitamin D hormone 1, 25-dihydroxyvitamin D.
10 es, but the interplay between the subsequent 1,25-dihydroxyvitamin D (1,25(OH)(2)D) and 24,25-dihydro
12 y metabolized to its hormonally active form, 1,25-dihydroxyvitamin D (1,25(OH)(2)D), by the 1-hydroxy
16 ion induced by the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25(OH)2D) with subsequent RNA
17 etween yearly 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D), and FGF23 serum le
18 (PTH) levels (2 degrees HPT), deficiency of 1,25-dihydroxyvitamin D (1,25(OH)2D), and hypocalciuria.
19 , we measured 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D), FGF23, and parathy
20 Synthesis of the active form of vitamin D, 1,25-dihydroxyvitamin D (1,25-(OH)(2)D), by renal epithe
21 ciations between serum levels of 25(OH)D and 1,25-dihydroxyvitamin D (1,25[OH](2)D) at baseline and t
22 tients with SS asthma were preincubated with 1,25-dihydroxyvitamin D (1,25[OH]2D [VitD]), followed by
23 in levels of 25-hydroxyvitamin D (25[OH]D), 1,25-dihydroxyvitamin D (1,25[OH]2D), parathyroid hormon
26 dies and mathematical modeling that hormonal 1,25-dihydroxyvitamin D (1,25D) and the vitamin D recept
27 N-gamma) and the calcitropic steroid hormone 1,25-dihydroxyvitamin D (1,25D) are activators of macrop
28 amin D, is converted into the active hormone 1,25-dihydroxyvitamin D (1,25D) by the cytochrome P450 e
30 factor 23 (FGF23), 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D (1,25D) predict renal outcomes i
31 fibroblast growth factor 23 (FGF23), reduced 1,25-dihydroxyvitamin D (1,25D), and hypophosphatemia.
32 most biologically active form of vitamin D, 1,25-dihydroxyvitamin D (1,25D), is synthesized by CYP27
34 ere relatively insensitive to treatment with 1,25-dihydroxyvitamin D (1,25D), the active form of vita
37 ting in synthesis of the pleiotropic hormone 1,25-dihydroxyvitamin D (1,25VD), which regulates over 6
38 tary fat intake (r = 0.29, P = 0.001), serum 1,25 dihydroxyvitamin D [1,25(OH)(2)D] concentrations (r
39 entrations of 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1, 25(OH)(2)D], intact parathyr
40 into 24,25-dihydroxyvitamin D(3) and active 1,25-dihydroxyvitamin D [1,25(OH)(2)D(3)], with subseque
42 signaling and increased serum phosphate and 1,25-dihydroxyvitamin D [1,25(OH)(2)D] concentrations in
43 iciency is related to serum 25(OH)D or serum 1,25-dihydroxyvitamin D [1,25(OH)(2)D] concentrations.
44 endent phosphate transport and production of 1,25-dihydroxyvitamin D [1,25(OH)(2)D] in the proximal t
47 Maternal 25(OH)D, parathyroid hormone, and 1,25-dihydroxyvitamin D [1,25(OH)(2)D] were determined a
48 nd serum calcium, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D [1,25(OH)(2)D], 24,25-dihydroxyv
49 entrations of 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25(OH)(2)D], and parathyroid
50 e circulating 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25(OH)(2)D], and their determ
51 able calcium pool, VO+, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D [1,25(OH)(2)D], parathyroid horm
52 anges in serum parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25(OH)2D] concentrations from
55 al VDR, serum 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25(OH)2D], and parathyroid ho
56 s, namely, 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)2D], have received the
57 D, genetic disorders of its bioactivation to 1,25-dihydroxyvitamin D [1,25(OH)2D], or disorders of vi
58 tamin D metabolism and inhibit production of 1,25-dihydroxyvitamin D [1,25(OH)2D], the active vitamin
61 c mice with losartan or paricalcitol (19-nor-1,25-dihydroxyvitamin D(2), an activated vitamin D analo
62 rmone-related peptide, prolactin, estradiol, 1,25-dihydroxyvitamin D, 24-hydroxyvitamin D, femoral bo
63 the hypothesis that calciotrophic hormones [1,25-dihydroxyvitamin D, 25-hydroxyvitamin D, and parath
66 own that the active metabolite of vitamin D, 1,25 dihydroxyvitamin D(3), stimulates differentiation a
68 se (HG, 25 mm) in the presence or absence of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) (25, 50 nm)
70 that the fat-soluble vitamin D(3) metabolite 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) and its nuc
72 keletal metabolism by inducing resistance to 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) by a mechan
76 o its calciotropic function, the secosteroid 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) has potent
78 function to maintain physiological levels of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) in the kidn
79 ropic effects, the active form of vitamin D, 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) is a potent
85 n important role in the maintenance of serum 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) under normo
89 n by fibroblast growth factor 23 (FGF23) and 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), and recipr
90 resistance to the active form of vitamin D [1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3))] who presen
91 ike multinucleated cell formation induced by 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) and parath
92 pothesis that the sunlight-dependent hormone 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) is a natur
93 synthesis, we proposed that vitamin D(3) and 1,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) may protec
94 Osteoclast formation, whether stimulated by 1,25-dihydroxyvitamin D(3) (1,25-D) or by parathyroid ho
96 differentiate to monocytes by an exposure to 1,25-dihydroxyvitamin D(3) (1,25D(3)), form a complex, a
97 AAT/enhancer-binding protein (C/EBP) beta in 1,25-dihydroxyvitamin D(3) (1,25D(3))-induced monocytic
100 n active ligand of vitamin D receptor (VDR), 1,25-dihydroxyvitamin D(3) (1,25D3), ameliorated experim
102 ere additive with that of melatonin whereas, 1,25-dihydroxyvitamin D(3) (IC(50)=10 nM), which by itse
106 oups were cultured in vitamin D-deficient or 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] -supplement
107 vestigated mechanisms by which genistein and 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] act synergi
108 is regulated by two major calcemic hormones, 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] and parathy
112 the 25-hydroxyvitamin D(3)-24-hydroxylase by 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] is well est
114 te cancer risk by lowering concentrations of 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], a hormone
117 tor that mediates the actions of its ligand, 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], which can
118 es a paracellular process, we found that the 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)]-activated g
120 in the spinal cord, so the locally-produced 1,25-dihydroxyvitamin D(3) accumulated and resolved the
122 D(3)-fed female mice had significantly more 1,25-dihydroxyvitamin D(3) and fewer CYP24A1 transcripts
124 data provide the first in vivo evidence that 1,25-dihydroxyvitamin D(3) and the VDR impact on ductal
125 tamin D(2), 24,25-dihydroxyvitamin D(3), and 1,25-dihydroxyvitamin D(3) could be detected in most sam
127 COS-1 cells with the Src-specific activator 1,25-dihydroxyvitamin D(3) enhanced activity; treatment
129 esearch has shown a strong protective effect 1,25-dihydroxyvitamin D(3) in experimental autoimmune en
130 nd TRPV6 null mice responded equally well to 1,25-dihydroxyvitamin D(3) in increasing intestinal calc
131 he vitamin D(3) receptor (VDR), whose ligand 1,25-dihydroxyvitamin D(3) is the biologically active fo
133 ked reductions in 25-hydroxyvitamin D(3) and 1,25-dihydroxyvitamin D(3) levels, despite upregulation
135 Finally, stimulation of Lyn expression by 1,25-dihydroxyvitamin D(3) treatment in HL-60 cells, a c
137 e the antiangiogenic activity of calcitriol (1,25-dihydroxyvitamin D(3)) in vivo and its effect on re
139 with the VDR activating ligand, calcitriol (1,25-dihydroxyvitamin D(3)), resulted in over a 6-fold i
141 y of CYP3A4, whose expression was induced by 1,25-dihydroxyvitamin D(3), and of CYP1A1, induced by be
142 growth-inhibited by all-trans-retinoic acid, 1,25-dihydroxyvitamin D(3), and transforming growth fact
143 ing in mouse marrow cultures stimulated with 1,25-dihydroxyvitamin D(3), as well as markers of osteoc
144 n circulating levels of parathyroid hormone, 1,25-dihydroxyvitamin D(3), or fibroblast growth factor
145 and fewer CYP24A1 transcripts, encoding the 1,25-dihydroxyvitamin D(3)-inactivating enzyme, in the s
150 s induced to differentiate by an exposure to 1,25-dihydroxyvitamin D(3); however, its activator in th
152 f prostate cancer through reduction of serum 1,25-dihydroxyvitamin D, a potent anti-prostate cancer h
154 irculating levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, alopecia persisted in the VDR-n
156 showed significantly higher serum levels of 1,25-dihydroxyvitamin D and developed extensive calcific
157 , hyperaldosteronism, and elevated levels of 1,25-dihydroxyvitamin D and Fgf23, consistent with disru
159 ke growth factor binding protein 3 but lower 1,25-dihydroxyvitamin D and parathyroid hormone concentr
160 ients, older patients had consistently lower 1,25-dihydroxyvitamin D and phosphate levels (p = .013 a
161 ient cardiac surgery-related fluctuations in 1,25-dihydroxyvitamin D and the aforementioned parameter
165 ns of change in calciotrophic hormones (PTH, 1,25-dihydroxyvitamin D, and 25-hydroxyvitamin D) in the
166 renal 1-alpha-hydroxylase expression, serum 1,25-dihydroxyvitamin D, and calcium levels than KL(fl/f
168 n kidney mass, lower concentrations of serum 1,25-dihydroxyvitamin D, and secondary increases in seru
169 FGF-23, soluble klotho, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and tartrate-resistant acid pho
170 blastic conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D appears to be an important posit
172 e concomitant with increased serum levels of 1,25-dihydroxyvitamin-D, as also observed in the Fgf23(-
173 hepcidin gene (HAMP) expression mediated by 1,25-dihydroxyvitamin D binding to the vitamin D recepto
174 We investigated whether administration of 1,25-dihydroxyvitamin D (calcitriol) to critically ill p
175 suggests that autocrine/paracrine actions of 1,25-dihydroxyvitamin D complement the classic endocrine
176 lase for de novo synthesis of a focally high 1,25-dihydroxyvitamin D concentration in the peripheral
179 baseline and 18 mo postparturition, PTH and 1,25-dihydroxyvitamin D concentrations did not decline,
181 ased levels of serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, consistent with decreased reabs
182 ith prohormone 25-hydroxyvitamin D or active 1,25-dihydroxyvitamin D decreased expression of hepcidin
184 ate 25-hydroxyvitamin D must be converted to 1,25-dihydroxyvitamin D for full biological activity, an
185 king elevations in serum PTH and calcitriol [1,25-dihydroxyvitamin D] in subjects consuming the low-p
188 lopecia was not secondary to toxic levels of 1,25-dihydroxyvitamin D interacting with an alternative
189 gate whether the markedly elevated levels of 1,25-dihydroxyvitamin D led to the alopecia, we raised V
190 tabolism was normalized in KO/TG mice: serum 1,25 dihydroxyvitamin D levels were higher in KO/TG mice
191 al bacterial populations, vitamin D receptor:1,25 dihydroxyvitamin D levels, epithelial barrier integ
192 t with hypercalciuria due to increased serum 1,25-dihydroxyvitamin D levels and increased intestinal
193 n with prediagnostic circulating 25(OH)D and 1,25-dihydroxyvitamin D levels and with two VDR single n
196 mine whether therapies aimed at treating low 1,25-dihydroxyvitamin D levels can improve the outcome i
197 for atherosclerosis, parathyroid hormone, or 1,25-dihydroxyvitamin D levels did not alter these assoc
199 calcium and parathyroid hormone levels, but 1,25-dihydroxyvitamin D levels that are inappropriately
200 ance for dietary magnesium intake, and serum 1,25-dihydroxyvitamin D levels was able to accurately se
201 (+/- SD) serum total 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D levels were 17 +/- 8 ng/mL and 3
203 menstruation, estradiol levels, PTH levels, 1,25-dihydroxyvitamin D levels, dietary calcium intake,
205 ve TaqI genotype (P = 0.005) and circulating 1,25-dihydroxyvitamin-D levels (P = 0.03) as independent
206 tal calcium, phosphate, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, magnesium, and markers of bone
207 MA, collagen type I and fibronectin, whereas 1,25-dihydroxyvitamin D markedly suppressed the inductio
208 stimulatory effect of 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D on related antibacterial protein
210 , alkaline phosphatase, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, parathyroid hormone, osteocalci
211 Treatment of neonatal cardiomyocytes with 1,25-dihydroxyvitamin D partially reduced isoproterenol-
214 by hyperphosphatemia, elevated production of 1,25-dihydroxyvitamin D, soft tissue calcifications, and
216 f phosphate and inhibits renal production of 1,25-dihydroxyvitamin D, thus helping to mitigate hyperp
217 se converts 25-hydroxyvitamin D [25(OH)D] to 1,25-dihydroxyvitamin D to regulate local innate immune
224 culated bioavailable 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were 2.5 +/- 2.0 ng/mL and 6.6 +