1 ed with ganciclovir who are not treated with calcium blockers.

2  by stratifying patients according to use of calcium blockers.

3  mM Ba2+ that were relatively insensitive to calcium blockers.

4 ation of cyclosporin A (CSA), phenytoin, and calcium blockers.

5 irus (CMV) infection and decreased by use of calcium blockers.

6 nsin-converting enzyme (ACE) inhibitors, and calcium blockers are commonly used for the treatment of

7 ibitor or receptor blocker, beta-blocker, or calcium blocker had no significant effect on survival.

8                                      Because calcium blockers have been shown to prevent TxCAD, we an

9 CoA reductase inhibitors, and the effects of calcium blockers in preventing TxCAD might have an immun

10  an alternative target anti-MCL therapy, and calcium blockers may be combined with bortezomib to over

11 en ganciclovir and placebo were compared: no calcium blockers (n=53), 32+/-11% (n=28) for ganciclovir

12 versus 62+/-16% (n=25) for placebo (P<0.03); calcium blockers (n=68), 50+/-14% (n=33) for ganciclovir

13                                To define the calcium blocker nature of the imidazo[2,1-b]thiazole-1,4

14 howed an increased sensitivity to the L-type calcium blocker nifedipine; SA node preparations stopped

15 luence of a calcium agonist (BAY K 8644) and calcium blockers on (+)- and (-)-epibatidine-induced ant

16 ed by calcium blockers, the combination of a calcium blocker (perillyl alcohol) with bortezomib suppr

17          When TG2 signaling was inhibited by calcium blockers, the combination of a calcium blocker (

18               Stratification on the basis of calcium blocker use revealed differences in TxCAD incide