ライフサイエンスコーパス: ara-A

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1 plasma 2-fluoro-arabinofuranosyladenine (2F-ara-A) concentration (its main metabolite); area under t

2 endent increase in Cmax and AUC(0-24h) of 2F-ara-A and achieved an AUC(0-24h) similar to intravenous

3 ses of F-AMP can achieve an AUC(0-24h) of 2F-ara-A similar to intravenous administration, with dose-i

4 Lastly, cells incubated with UCN-01 before F-ara-A addition did not arrest in S-phase.

5 Thus, the DNA damage induced by F-ara-A initiated a hierarchical regulatory cascade throug

6 ools were depressed after incubation of Cl-F-ara-A for 3 h and only partially recovered following was

7 was not reversed 72 h after removal of Cl-F-ara-A from the medium.

8 mphoblastoid CEM cells was inhibited by Cl-F-ara-A in a concentration-dependent manner that was not r

9 fluoro-beta-D-arabinofuranosyl)adenine (Cl-F-ara-A) on DNA synthesis was evaluated both in whole cell

10 f CDP reduction in cells incubated with Cl-F-ara-A; reduction of ADP, GDP, and UDP were affected to l

11 This assay was used to determine F-ara-A-induced apoptosis in different lymphocyte subsets

12 d enhanced the sensitivity to fludarabine (F-ara-A) of CLL cells lacking functional p53.

13 iously that the nucleoside of fludarabine (F-ara-A), a clinically effective agent against chronic lym

14 Fludarabine (F-ara-A), an adenine nucleoside analog with efficacy in B-

15 logue 9-beta-D-arabinosyl-2-fluoroadenine (F-ara-A).

16 gainst JNK1 mRNA resulted in a decrease in F-ara-A-induced apoptosis.

17 reatment of ML-1 cells with 3 or 10 microM F-ara-A specifically killed cells in the S-phase of the po

18 concentrations of fludarabine nucleoside (F-ara-A) by instituting an arrest in S-phase that involved

19 When incorporation of F-ara-A into DNA was blocked by pretreatment of the cells

20 lts suggested a direct apoptotic effect of F-ara-A on B-CLL lymphocytes that decreases with increasin

21 We observed a direct effect of F-ara-A on both B-CLL and T lymphocytes.

22 F-ara-ATP, the nucleoside triphosphate of F-ara-A, into DNA resulted in the activation of JNK1 in a

23 t that JNK1 is involved in transduction of F-ara-A-induced distress signals into an apoptotic respons

24 was found between bcl-2 and spontaneous or F-ara-A-induced apoptosis.

25 53-deficient CLL cells to CD95-mediated or F-ara-A-induced apoptosis.

26 The response to F-ara-A in B-CLL lymphocytes in vitro was Rai stage-depend

27 d and CD95 and enhanced the sensitivity to F-ara-A of p53-deficient CLL cells.

28 hibitor 7-hydroxystaurosporine (UCN-01) to F-ara-A-arrested S-phase cells resulted in a rapid decreas

29 late-stage disease were more sensitive to F-ara-A-induced apoptosis.

30 patients and normal controls treated with F-ara-A in vitro.

31 ine (6-AAP) was synthesized as a prodrug for ara-A that utilizes the azide reduction biotransformatio

32 life of ara-A was 7-14 times higher than for ara-A administered intravenously.

33 6-AAP was synthesized from ara-A via its 6-chloro analogue 4.

34 rain after the intravenous administration of ara-A.

35 sing the half-life and the brain delivery of ara-A.

36 The in vivo metabolism and disposition of ara-A and 6-AAP were conducted in mice.

37 or intravenous route), significant levels of ara-A were found in the brain.

38 r oral or intravenous route,the half-life of ara-A was 7-14 times higher than for ara-A administered

39 study demonstrate that 6-AAP is converted to ara-A, potentially increasing the half-life and the brai

40 n of the azido moiety to the amine, yielding ara-A.

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