Preinduction cervical softening with endocervical PGE2 gel. A multi-center trial.

In a prospective, randomized trial, a single dose of PGE2 gel, 0.5 mg (2.5 ml), was given to 416 low Bishop Score patients 12 h prior to indicated oxytocin induction and compared with 404 non-gel controls. Successful initial induction was achieved in 83% of the treated and 58% of the non-treated subjects. In addition the induction-delivery interval was shortened (median times 9.0 h vs. 11.3 h) and fewer cesarean sections were performed (16% vs. 21%) in the PGE2 gel series. The endocervical administration of PGE2 was well tolerated and, provided care is taken to avoid excess extra-amniotic placement, systemic PGE2 effects are minimal.

Cell proliferation kinetics and drug sensitivity of exponential and stationary populations of cultured L1210 cells.

Drug sensitivity and cell cycle parameters of L1210 cells in culture in exponential (10(5) to 4 x 10(5) cells/ml) and plateau phase (greater than 8 x 10(5) cells/ml) of growth were compared. The percentage of cells in G1, S, and G2 + M for exponential and plateau-phase cultures was 24.1, 70.0, and 5.9, and 42.5, 45.6, and 11.9, respectively. These values correspond to those reported previously for early and late L1210 mouse leukemia cells. Cell survival (measured by cloning) after drug exposure showed that actinomycin D, 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea, chlorozotocin, and streptozocin were all equally lethal to cells in both phases, and 1-beta-D-arabinofuranosylcytosine, high-specific-activity (20Ci/mmole) [3H]thymidine, vincristine, daunomycin, adriamycin, and 5-fluorouracil were more lethal to exponential cells than to plateau-phase cells. The percentage kill by S-phase-specific agents such as 1-beta-D-arabinofuranosylcytosine and[3H]thymidine corresponded well with the percentage of cells in S. Finally, 1,3-bis(2-chloroethyl)-1-nitrosourea was more toxic to plateau cells than to exponential cells.

Use of cell-cycle information in the preparation of drug combinations: results with cytosine arabinoside plus actinomycin D1,2.

Cytosine arabinoside (ara-C) plus actinomycin D acted synergistically in killing L1210 and DON cells. The time course of cell-kill by the combination was different from that seen for either drug alone. The results obtained (both with L1210 and synchronous DON cells) suggest that cells blocked in G1/S with continuing unbalanced growth are particularly sensitive to the combined action of ara-C and actinomycin D.