Background The study was conducted to evaluate the impact of out-of-pocket expense on intrauterine device (IUD) utilization among women with private insurance. Study Design We reviewed the records of all women with private insurance who requested an IUD for contraception from an urban academic gynecology practice from May 2007 through April 2008. For each patient, we determined the out-of-pocket expense that would be incurred, and whether she ultimately had an IUD placed. The total charge for placement of a copper or levonorgestrel IUD (including the device) was $815. Results Ninety-five women requested an IUD during the study period. The distribution of out-of-pocket expense was bimodal: less than $50 for 35 (37%) women and greater than $500 for 52 (55%) women. IUD insertion occurred in 24 (25%) women, 19 of whom had an out-of-pocket expense less than $50. In univariate and multivariable analysis, women with insurance coverage that resulted in less than $50 out-of-pocket expense for the IUD were more likely to have an IUD placed than women required to pay $50 or more (adjusted OR=11.4, 95% CI = 3.6, 36.6),. Conclusions Women requesting an IUD for contraception are significantly more likely to have an IUD placed when out-of-pocket expense is less than $50.

The myristoylated alanine-rich C kinase substrate (MARCKS) is a primary substrate of protein kinase C (PKC) thought to regulate membrane-filamentous actin cytoskeletal plasticity in response to PKC activity in the regulation of synaptic efficacy. We have recently reported that MARCKS expression is significantly elevated (45%) in the hippocampus of DBA/2J mice, which exhibit impaired hippocampus-dependent learning and hippocampal long-term potentiation (LTP), compared with C57BL/6J mice. The latter finding led us to hypothesize that elevations in MARCKS expression are detrimental to hippocampal plasticity and function. To assess this more directly, we examined hippocampal (CA1) paired-pulse facilitation and LTP, and hippocampus-dependent learning in mice overexpressing MARCKS through the expression of a human MARCKS transgene (Tg+). The human MARCKS protein was confirmed to be expressed in the hippocampus of Tg+ mice but not in Tg- mice. Schaffer collateral paired-pulse facilitation, input-output responses, and LTP did not differ between Tg+ and Tg- mice, indicating that neurotransmitter release, short-term, and long-term synaptic plasticity are not impaired by MARCKS overexpression. In the Morris water maze, Tg+ mice exhibited a mild but significant spatial learning impairment during initial acquisition, and a more severe impairment during reversal training. Tg+ did not exhibit impaired swim speed or visible platform performance relative to Tg- mice, indicating the absence of gross sensorimotor deficits. Fear conditioning to either context or cue was not impaired in Tg+ mice. Behavioral deficits could not be attributed to differences in hippocampal PKC isozyme (alpha beta(II), gamma, epsilon, zeta) or calmodulin expression, or alterations in hippocampal cytoarchitecture or infrapyramidal mossy fiber limb length. Collectively, these results indicate that elevations in MARCKS expression are detrimental to specific aspects of hippocampal function.