ライフサイエンスコーパス: cilostazol

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1 heir sensitivities to inhibition by cGMP and cilostazol.

2 ction, and the phosphodiesterase 3 inhibitor cilostazol.

3 muM) and the phosphodiesterase-3 inhibitors cilostazol (10 muM) and milrinone (2.5 muM) restored ele

4 l/L) or the phosphodiesterase III inhibitors cilostazol (10 mumol/L) or milrinone (5 mumol/L) diminis

5 antation to receive, in addition to aspirin, cilostazol 100 mg BID or placebo for 6 months; clopidogr

6 nequally (2:1) to 12 weeks of treatment with cilostazol 100 mg PO BID or placebo.

7 lacebo-controlled trial to determine whether cilostazol, a drug that suppresses intimal proliferation

8 In this study, we assessed whether cilostazol, a phosphodiesterase III inhibitor, could pro

9 d elevated CD39 protein (2-fold [P<0.05] for cilostazol and 2.5-fold [P<0.01] for milrinone), while m

10 lecular models show that the PDE3 inhibitors cilostazol and milrinone share some of common residues b

11 HUVEC ATPase activity increased by 25% with cilostazol and milrinone treatment (P<0.05 and P<0.01, r

12 UVECs) were treated with the PDE3 inhibitors cilostazol and milrinone, then analyzed using qRT-PCR, i

13 Cilostazol and sildenafil did not have negative pharmaco

14 Cilostazol and sildenafil may benefit tuberculosis patie

15 rance in the lung, while the addition of the cilostazol and sildenafil reduced the time to clearance

16 pharmacokinetic interactions between PDE-Is (cilostazol and sildenafil) and rifampin.

17 ance, and relapse when types 3 and 5 PDE-Is (cilostazol and sildenafil, respectively) and rolipram we

18 or angiotensin receptor blockers [ARBs], and cilostazol) and lifestyle counseling (exercise or diet c

19 anscription, inhibitors of PDE3 (siguazodan, cilostazol) and PDE4 (rolipram, GSK256066, roflumilast N

20 Quinidine, cilostazol, and milrinone suppress the hypothermia-induc

21 and examines the effectiveness of quinidine, cilostazol, and milrinone to prevent hypothermia-induced

22 A, F972A and Q975A showed increased K(i) for cilostazol but no difference for milrinone from the reco

23 enosis or a sham operation and fed normal or cilostazol diet for three months.

24 the PDE3 selective inhibitors milrinone and cilostazol each suppressed thrombin-induced cAMP-depende

25 oup clinical trial evaluated the efficacy of cilostazol for treatment of stable, moderately severe in

26 rowing, occurred in 22.0% of patients in the cilostazol group and in 34.5% of the placebo group (P=0.

27 Cilostazol improved walking distances, significantly inc

28 SE: 2.4%), ACEI/ARB in 28.4% (SE: 2.0%), and cilostazol in 4.7% (SE: 1.0%) of visits.

29 also assessing medical therapies, including cilostazol, in patients with intracranial stenosis.

30 Cilostazol is a new phosphodiesterase inhibitor that sup

31 The data suggest cilostazol is safe and well tolerated for the treatment

32 the mutants), and diminished sensitivity to cilostazol (K(i) of the mutants were 18- to 371-fold hig

33 d for each experiment based on solubility of cilostazol, milrinone, and 8-Br-cAMP.

34 Supervised exercise programs and cilostazol remain the first-line medical therapies for c

35 Treatment with the drug cilostazol resulted in a significantly larger minimal lu

36 nonconserved T844 may be responsible for the cilostazol selectivity of PDE3A.

37 Altogether cilostazol showed potential to ameliorate the gliovascul

38 ition of the mutant enzymes by milrinone and cilostazol, specific inhibitors of PDE3.

39 and the well-characterized PDE3A inhibitor, cilostazol, to modulate 3',5'-cyclic adenosine monophosp

40 Restenosis was significantly lower in cilostazol-treated diabetics (17.7% versus 37.7%, P=0.01

41 sions after hypoperfusion was reduced in the cilostazol-treated group.

42 ments in walking performance observed in the cilostazol-treated group.

43 The minimal luminal diameter at 6 months for cilostazol-treated patients was 1.77 mm for the analysis

44 Cilostazol treatment reduced the impairment in working m

45 d after hypoperfusion, were ameliorated with cilostazol treatment.

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