ライフサイエンスコーパス: calcemic

コーパス検索結果 (１語後でソート)

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1 ic ablation of this gene in mice leads to no calcemic abnormalities.

2 t compounds dissociate antiproliferative and calcemic activities of 1,25(OH)2D3, but the molecular ba

3 d vitamin D compounds (5-16) exhibit reduced calcemic activity both in bone and in the intestine.

4 dene vitamins are characterized by very high calcemic activity in rats.

5 high transcriptional activity with also low calcemic activity in vivo.

6 vitamin D3 is hypercalcemia, we examined the calcemic activity of 1,25(OH)2-16-ene-5,6-trans-D3 in mi

7 In conclusion, the low calcemic activity of 19-norD(2) seems to be due to an ac

8 The in vivo tests have revealed that the calcemic activity of all analogues in the E-series (5a,

9 is hypercalcemia, and therefore, we examined calcemic activity of Ro 27-2014 in mice and found it not

10 h a 2-methylene substituent showed selective calcemic activity profiles, being extremely effective on

11 ure patients and in uremic rats but has less calcemic activity than 1,25(OH)(2)D(3).

12 athyroid hormone effectively, but with lower calcemic activity than 1,25(OH)(2)D(3).

13 ion and reduced telomerase activity with low calcemic activity, suggesting further testing in in vivo

14 CYP24 inhibitor (IC(50) = 7.4 nM) having low calcemic activity.

15 by topical application of vitamin D3 or low-calcemic analogues.

16 her DBP levels have causal effects on common calcemic and cardiometabolic disease.

17 alization assays, and induced more prolonged calcemic and phosphate responses in mice.

18 o be associated with prolonged physiological calcemic and phosphate responses.

19 d hormone synthesis and secretion with lower calcemic and phosphatemic activities.

20 6-ene-5,6-trans-D3 was at least 40-fold less calcemic as compared with 1,25(OH)2D3 and 1,25(OH)2-16-e

21 hyperproliferative disorders is hampered by calcemic effects, hence the continuous development of ch

22 n vivo, the three analogues had markedly low calcemic effects.

23 D receptor (VDR) mediates the effects of the calcemic hormone 1alpha,25-dihydroxyvitamin D3 [1,25(OH)

24 , RANKL expression is regulated by two major calcemic hormones, 1,25-dihydroxyvitamin D(3) [1,25(OH)(

25 3b and oxime ether 4b are considerably less calcemic (i.e., safer) than calcitriol (1).

26 icity (hypercalcemia), ketone 2b is strongly calcemic in rats, whereas oxime 3b and oxime ether 4b ar

27 ntiproliferative in vitro and desirably less calcemic in vivo than the natural hormone.

28 ally, these nonsecosteroidal VDRMs were less calcemic in vivo, and LY2108491 exhibited more than 270-

29 ongly antiproliferative in vitro but are low-calcemic in vivo.

30 chain resulted in a progressive increase in calcemic liability.

31 ols to 290 nmol/L, without inducing signs of calcemic or bone toxicity, and significantly reduced dia

32 ods to determine the causal effect of DBP on calcemic (osteoporosis and hyperparathyroidism) and card

33 ever, the in vivo assays indicated only weak calcemic potency of these compounds in the intestinal ca

34 he potential therapeutic utility of its less calcemic precursor, 25-hydroxyvitamin D3 [25(OH)D3], whi

35 potential mechanisms to explain the reduced calcemic response to 19-norD(2).

36 ention on mechanisms that underlie the acute calcemic response to PTH and factors, such as blood phos

37 Calcemic responses, 0.5-10 hours after intraperitoneal i

38 skeletal mineralization and suggest that its calcemic role can be mostly compensated by CaBP-D9k.

39 es in the NOD mouse but also elicit unwanted calcemic side effects.

40 In contrast, 1,25(OH)2D3 was more calcemic than 1,25(OH)2-16-ene-5,6-trans-D3.

41 ontrol parathyroid hormone secretion and non-calcemic vitamin D analogs.

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